| 2866674 |
18976 |
Pomc
|
Analgesia |
We have shown that a number of compounds which inhibit the degradation of met-enkephalin can produce naloxone-reversible analgesia in mice. |
| 16224585 |
18610 |
Pdyn
|
Analgesia |
We studied the effect of acupuncture analgesia on the expression of ppENKmRNA, MEK-IR, and Dyn-IR in circulating mouse lymphocytes. |
| 16224585 |
17242 |
Mdk
|
Analgesia |
We studied the effect of acupuncture analgesia on the expression of ppENKmRNA, MEK-IR, and Dyn-IR in circulating mouse lymphocytes. |
| 19607689 |
18976 |
Pomc
|
Analgesia |
Substance P and beta-endorphin mediate electro-acupuncture induced analgesia in mouse cancer pain model |
| 19607689 |
18976 |
Pomc
|
Analgesia |
It also indicated that EA treatment could be used as an alternative therapeutic method for cancer pain due to a consequent decrease in substance P and increase in beta-endorphin levels. |
| 19607689 |
21333 |
Tac1
|
Analgesia |
Substance P and beta-endorphin mediate electro-acupuncture induced analgesia in mouse cancer pain model |
| 19607689 |
21333 |
Tac1
|
Analgesia |
Also, the overexpression of pain peptide substance P in the dorsal horn of the spinal cord was significantly decreased in the EA-treated group compared to the tumor control on Day 9 post inoculation. |
| 19607689 |
21333 |
Tac1
|
Analgesia |
It also indicated that EA treatment could be used as an alternative therapeutic method for cancer pain due to a consequent decrease in substance P and increase in beta-endorphin levels. |
| 19607689 |
21333 |
Tac1
|
Analgesia |
4A, substance P was overexpressed in the tumor control group compared to that of the normal control, suggesting that the tumor mass could activate neuropathic pain-related proteins. |
| 19607689 |
21333 |
Tac1
|
Analgesia |
On the contrary, EA treatment for 9 days effectively reduced the expression of pain peptide substance P in the dorsal horn section of the spinal cord of mice compared to the untreated tumor control group. |
| 22524543 |
11539 |
Adora1
|
Analgesia |
Likewise, in the spared nerve injury (SNI) model of neuropathic pain, hPAP (250 mU) inhibited thermal and mechanical hypersensitivity for three days in the ipsilateral (injured) hindpaw of wild-type mice but not A1R-/- mice (Figure 4C,D). |
| 22524543 |
11539 |
Adora1
|
Analgesia |
Collectively, these data indicate that hPAP has localized, long-lasting, A1R-dependent antinociceptive effects in two models of chronic pain when injected peripherally. |
| 22524543 |
11539 |
Adora1
|
Analgesia |
To determine if peripheral injection of hPAP could preemptively inhibit pain hypersensitivity, as occurs when hPAP is injected intrathecally, we injected hPAP (250 mU) into the popliteal fossa of wild-type and A1R-/- mice and performed the SNI surgery the following day. |
| 22524543 |
11539 |
Adora1
|
Analgesia |
Antinociception could be transiently boosted with additional substrate (AMP) or transiently blocked with an A1R antagonist or an inhibitor of phospholipase C. This novel therapeutic approach:which we term PAPupuncture:locally inhibits pain for an extended period of time (100x acupuncture), exploits a molecular mechanism that is common to acupuncture, yet does not require acupuncture needle stimulation. |
| 22524543 |
11539 |
Adora1
|
Analgesia |
Here, we found that injection of PAP into the popliteal fossa:a space behind the knee that encompasses the Weizhong acupuncture point:had dose- and A1R-dependent antinociceptive effects in mouse models of acute and chronic pain. |
| 22524543 |
56318 |
Acp3
|
Analgesia |
Likewise, in the spared nerve injury (SNI) model of neuropathic pain, hPAP (250 mU) inhibited thermal and mechanical hypersensitivity for three days in the ipsilateral (injured) hindpaw of wild-type mice but not A1R-/- mice (Figure 4C,D). |
| 22524543 |
56318 |
Acp3
|
Analgesia |
In both chronic pain models, ipsilateral hPAP injections had no effects in the contralateral (non-inflamed/non-injured) hindpaw (Figure 4A-D). |
| 22524543 |
56318 |
Acp3
|
Analgesia |
Collectively, these data indicate that hPAP has localized, long-lasting, A1R-dependent antinociceptive effects in two models of chronic pain when injected peripherally. |
| 22524543 |
56318 |
Acp3
|
Analgesia |
To determine if peripheral injection of hPAP could preemptively inhibit pain hypersensitivity, as occurs when hPAP is injected intrathecally, we injected hPAP (250 mU) into the popliteal fossa of wild-type and A1R-/- mice and performed the SNI surgery the following day. |
| 22524543 |
56318 |
Acp3
|
Analgesia |
Here, we found that injection of PAP into the popliteal fossa:a space behind the knee that encompasses the Weizhong acupuncture point:had dose- and A1R-dependent antinociceptive effects in mouse models of acute and chronic pain. |
| 23365600 |
79212 |
Slc6a1
|
Analgesia |
We conclude that inhibition of GAT1 function will strengthen the inhibitory action of the GABAergic system and hence may contribute to acupuncture-induced analgesia. |
| 23365600 |
25601 |
Oprm1
|
Analgesia |
Among the several canonical opioid receptors, muOR has the highest affinity with morphine; studies with muOR knockout mice also show that muOR is necessary for morphine-induced analgesia and other symptoms. |
| 23365600 |
24613 |
Oprd1
|
Analgesia |
Notably, the physical interactions between muOR and deltaOR may contribute to long-term changes of morphine-induced analgesia. |
| 23365600 |
25601 |
Oprm1
|
Analgesia |
Notably, the physical interactions between muOR and deltaOR may contribute to long-term changes of morphine-induced analgesia. |
| 24524846 |
26417 |
Mapk3
|
Analgesia |
Second, in mouse pain models using formalin and complete Freund adjuvant, we found that acupuncture attenuated the nociceptive behavior and the mechanical allodynia; these effects were blocked when ERK cascade was interrupted by the mitogen-activated protein kinase kinase (MEK)/mitogen-activated protein kinase (MAPK) inhibitor U0126 (.8 mug/muL). |
| 24524846 |
26413 |
Mapk1
|
Analgesia |
Second, in mouse pain models using formalin and complete Freund adjuvant, we found that acupuncture attenuated the nociceptive behavior and the mechanical allodynia; these effects were blocked when ERK cascade was interrupted by the mitogen-activated protein kinase kinase (MEK)/mitogen-activated protein kinase (MAPK) inhibitor U0126 (.8 mug/muL). |
| 24524846 |
26417 |
Mapk3
|
Analgesia |
Based on these results, we suggest that ERK phosphorylation following acupuncture needling is a biochemical hallmark initiating the effect of acupuncture including analgesia. |
| 24524846 |
26413 |
Mapk1
|
Analgesia |
Based on these results, we suggest that ERK phosphorylation following acupuncture needling is a biochemical hallmark initiating the effect of acupuncture including analgesia. |
| 24524846 |
26417 |
Mapk3
|
Analgesia |
This article presents the novel evidence of the local molecular signaling in acupuncture analgesia by demonstrating that ERK activation in the skin layer contributes to the analgesic effect of acupuncture in a mouse pain model. |
| 24524846 |
26413 |
Mapk1
|
Analgesia |
This article presents the novel evidence of the local molecular signaling in acupuncture analgesia by demonstrating that ERK activation in the skin layer contributes to the analgesic effect of acupuncture in a mouse pain model. |
| 24524846 |
26417 |
Mapk3
|
Analgesia |
To examine whether acupuncture-induced ERK activation is involved in the analgesic effects of acupuncture, we used the MEK/MAPK inhibitor U0126 in the formalin-induced and CFA-induced mouse pain model. |
| 24524846 |
26413 |
Mapk1
|
Analgesia |
To examine whether acupuncture-induced ERK activation is involved in the analgesic effects of acupuncture, we used the MEK/MAPK inhibitor U0126 in the formalin-induced and CFA-induced mouse pain model. |
| 24524846 |
26417 |
Mapk3
|
Analgesia |
Finally, we investigated whether local ERK activation caused by acupuncture needling was linked to analgesia using the formalin-induced and CFA-induced pain models. |
| 24524846 |
26413 |
Mapk1
|
Analgesia |
Finally, we investigated whether local ERK activation caused by acupuncture needling was linked to analgesia using the formalin-induced and CFA-induced pain models. |
| 24524846 |
26417 |
Mapk3
|
Analgesia |
From Peripheral to Central: The Role of ERK Signaling Pathway in Acupuncture Analgesia |
| 24524846 |
26413 |
Mapk1
|
Analgesia |
From Peripheral to Central: The Role of ERK Signaling Pathway in Acupuncture Analgesia |
| 24524846 |
17242 |
Mdk
|
Analgesia |
Second, in mouse pain models using formalin and complete Freund adjuvant, we found that acupuncture attenuated the nociceptive behavior and the mechanical allodynia; these effects were blocked when ERK cascade was interrupted by the mitogen-activated protein kinase kinase (MEK)/mitogen-activated protein kinase (MAPK) inhibitor U0126 (.8 mug/muL). |
| 24524846 |
17242 |
Mdk
|
Analgesia |
To examine whether acupuncture-induced ERK activation is involved in the analgesic effects of acupuncture, we used the MEK/MAPK inhibitor U0126 in the formalin-induced and CFA-induced mouse pain model. |
| 27381504 |
14810 |
Grin1
|
Analgesia |
N-methyl-D-aspartate receptor (NMDAR) activation and downstream transduction pathways are crucial for pain signalling. |
| 27381504 |
14810 |
Grin1
|
Analgesia |
We examined the contributions of NMDAR signalling to FM pain and EA responses in a mouse model. |
| 29981376 |
12846 |
Comt
|
Analgesia |
Patients with chronic overlapping pain conditions have decreased levels of catechol-O-methyltransferase (COMT), an enzyme that metabolizes catecholamines. |
| 29981376 |
12846 |
Comt
|
Analgesia |
Consistent with clinical syndromes, we previously demonstrated that COMT inhibition in rodents produces persistent pain and heightened immune responses. |
| 29981376 |
12846 |
Comt
|
Analgesia |
Following COMT inhibition, MRL/MpJ mice had more pronounced pain. |
| 29981376 |
26416 |
Mapk14
|
Analgesia |
The p38 MAPK is an important mediator of persistent pain and inflammation. |
| 31447579 |
26416 |
Mapk14
|
Analgesia |
Inhibition of SP signaling pathway or activity of p38 MAPK significantly improved the EA analgesia In EA poor-responders with SCD, which provides a promising way to treat the chronic pain in patients with SCD. |
| 31447579 |
26416 |
Mapk14
|
Analgesia |
Interestingly, poor responders exhibited high levels of substance P (SP), a mediator of chronic pain, as well as active p38 MAPK in spinal cords. |
| 31447579 |
26416 |
Mapk14
|
Analgesia |
The present study aimed to investigate the roles of inhibition of SP and SP-activated p38 MAPK in chronic pain in sickle mice that are poorly responsive to EA intervention (moderate/non-responders). |
| 31447579 |
26416 |
Mapk14
|
Analgesia |
Results: In EA poor-responders, combined treatment with EA and netupitant significantly enhanced the analgesic effects of EA in poor-responders on mechanical, heat, cold, and deep tissue pain, and decreased phosphorylation of p38 MAPK in lumbar spinal cords and its nuclear translocation in the spinal dorsal horn. |
| 31447579 |
21333 |
Tac1
|
Analgesia |
Interestingly, poor responders exhibited high levels of substance P (SP), a mediator of chronic pain, as well as active p38 MAPK in spinal cords. |
| 31447579 |
21333 |
Tac1
|
Analgesia |
The present study aimed to investigate the roles of inhibition of SP and SP-activated p38 MAPK in chronic pain in sickle mice that are poorly responsive to EA intervention (moderate/non-responders). |
| 31447579 |
21333 |
Tac1
|
Analgesia |
Conclusions: These results suggest a pivotal role of SP in maintaining the chronic pain in SCD via spinal phospho-p38 MAPK signaling, which may hinder the effect of EA in poor responders. |
| 31447579 |
21333 |
Tac1
|
Analgesia |
Inhibition of SP signaling pathway or activity of p38 MAPK significantly improved the EA analgesia In EA poor-responders with SCD, which provides a promising way to treat the chronic pain in patients with SCD. |
| 31447579 |
26416 |
Mapk14
|
Analgesia |
Conclusions: These results suggest a pivotal role of SP in maintaining the chronic pain in SCD via spinal phospho-p38 MAPK signaling, which may hinder the effect of EA in poor responders. |
| 31447579 |
21333 |
Tac1
|
Analgesia |
Substance P modulates electroacupuncture analgesia in humanized mice with sickle cell disease |
| 31941349 |
193034 |
Trpv1
|
Analgesia |
AIMS: We hypothesised that acupuncture would reduce FM pain by influencing transient receptor potential cation channel subfamily V member 1 (TRPV1) and the downstream phosphorylated extracellular signal-regulated kinases (pERK), which are located in the central thalamus, amygdala and cortex. |
| 31941349 |
193034 |
Trpv1
|
Analgesia |
Electroacupuncture reduces fibromyalgia pain by downregulating the TRPV1-pERK signalling pathway in the mouse brain. |
| 32796318 |
74104 |
Abcb6
|
Analgesia |
One-way ANOVA with the Newman-Keuls post hoc test for Nr4a1 (F[2, 6] = 28.15, P = 0.0009), Rasgrp1 (F[2, 6] = 21.31, P = 0.0019), Rassf1 (F[2, 6] = 13.52, P = 0.0060), Chkb (F[2, 6] = 18.22, P = 0.0028), Tekt4 (F[2, 6] = 9.661, P = 0.0133), and Abcb6 (F[2, 6] = 3.840, P = 0.0844) in mice with PSNL-induced neuropathic pain demonstrated that AP treatment significantly decreased the mRNA expression levels in the PFC (Nr4a1, P < 0.001; Rasgrp1, P < 0.01; Rassf1, P < 0.01; Chkb, P < 0.01; Tekt4, P < 0.01; Abcb6, P < 0.01 vs PSNL; Figs. |
| 32796318 |
12651 |
Chkb
|
Analgesia |
These results suggest that acupuncture can relieve chronic pain-induced comorbid conditions by altering DNA methylation of Nr4a1, Rasgrp1, Rassf1, and Chkb in the PFC. |
| 32796318 |
12651 |
Chkb
|
Analgesia |
One-way ANOVA with the Newman-Keuls post hoc test for Nr4a1 (F[2, 6] = 28.15, P = 0.0009), Rasgrp1 (F[2, 6] = 21.31, P = 0.0019), Rassf1 (F[2, 6] = 13.52, P = 0.0060), Chkb (F[2, 6] = 18.22, P = 0.0028), Tekt4 (F[2, 6] = 9.661, P = 0.0133), and Abcb6 (F[2, 6] = 3.840, P = 0.0844) in mice with PSNL-induced neuropathic pain demonstrated that AP treatment significantly decreased the mRNA expression levels in the PFC (Nr4a1, P < 0.001; Rasgrp1, P < 0.01; Rassf1, P < 0.01; Chkb, P < 0.01; Tekt4, P < 0.01; Abcb6, P < 0.01 vs PSNL; Figs. |
| 32796318 |
13433 |
Dnmt1
|
Analgesia |
Next, to confirm the changes in DNMT enzymes associated with acupuncture treatment (3 days/week for 6 months) for PSNL-induced neuropathic pain, DNMT1, DNMT3a, and DNMT3b were examined by Western blot analysis in the PFC tissues of the mouse model. |
| 32796318 |
13433 |
Dnmt1
|
Analgesia |
Next, to confirm the changes in DNMT enzymes associated with acupuncture treatment (3 days/week for 6 months) for PSNL-induced neuropathic pain, DNMT1, DNMT3a, and DNMT3b were examined by Western blot analysis in the PFC tissues of the mouse model. |
| 32796318 |
13435 |
Dnmt3a
|
Analgesia |
Next, to confirm the changes in DNMT enzymes associated with acupuncture treatment (3 days/week for 6 months) for PSNL-induced neuropathic pain, DNMT1, DNMT3a, and DNMT3b were examined by Western blot analysis in the PFC tissues of the mouse model. |
| 32796318 |
13436 |
Dnmt3b
|
Analgesia |
Next, to confirm the changes in DNMT enzymes associated with acupuncture treatment (3 days/week for 6 months) for PSNL-induced neuropathic pain, DNMT1, DNMT3a, and DNMT3b were examined by Western blot analysis in the PFC tissues of the mouse model. |
| 32796318 |
17257 |
Mecp2
|
Analgesia |
One-way ANOVA with the Newman-Keuls post hoc test for 5-mC- (F[3, 20] = 16.07, P < 0.0001) and MeCP2-positive NeuN cells (F[3, 20] = 34.71, P < 0.0001) in mice with PSNL-induced neuropathic pain demonstrated that AP treatment significantly increased global DNA methylation in the PFC (5-mC, P < 0.001; MeCP2, P < 0.001 vs PSNL), but DNA methylation in the PFC was not changed in the CP group compared to that in the PSNL group (Figs. |
| 32796318 |
52897 |
Rbfox3
|
Analgesia |
One-way ANOVA with the Newman-Keuls post hoc test for 5-mC- (F[3, 20] = 16.07, P < 0.0001) and MeCP2-positive NeuN cells (F[3, 20] = 34.71, P < 0.0001) in mice with PSNL-induced neuropathic pain demonstrated that AP treatment significantly increased global DNA methylation in the PFC (5-mC, P < 0.001; MeCP2, P < 0.001 vs PSNL), but DNA methylation in the PFC was not changed in the CP group compared to that in the PSNL group (Figs. |
| 32796318 |
15370 |
Nr4a1
|
Analgesia |
These results suggest that acupuncture can relieve chronic pain-induced comorbid conditions by altering DNA methylation of Nr4a1, Rasgrp1, Rassf1, and Chkb in the PFC. |
| 32796318 |
15370 |
Nr4a1
|
Analgesia |
One-way ANOVA with the Newman-Keuls post hoc test for Nr4a1 (F[2, 6] = 28.15, P = 0.0009), Rasgrp1 (F[2, 6] = 21.31, P = 0.0019), Rassf1 (F[2, 6] = 13.52, P = 0.0060), Chkb (F[2, 6] = 18.22, P = 0.0028), Tekt4 (F[2, 6] = 9.661, P = 0.0133), and Abcb6 (F[2, 6] = 3.840, P = 0.0844) in mice with PSNL-induced neuropathic pain demonstrated that AP treatment significantly decreased the mRNA expression levels in the PFC (Nr4a1, P < 0.001; Rasgrp1, P < 0.01; Rassf1, P < 0.01; Chkb, P < 0.01; Tekt4, P < 0.01; Abcb6, P < 0.01 vs PSNL; Figs. |
| 32796318 |
19419 |
Rasgrp1
|
Analgesia |
These results suggest that acupuncture can relieve chronic pain-induced comorbid conditions by altering DNA methylation of Nr4a1, Rasgrp1, Rassf1, and Chkb in the PFC. |
| 32796318 |
19419 |
Rasgrp1
|
Analgesia |
One-way ANOVA with the Newman-Keuls post hoc test for Nr4a1 (F[2, 6] = 28.15, P = 0.0009), Rasgrp1 (F[2, 6] = 21.31, P = 0.0019), Rassf1 (F[2, 6] = 13.52, P = 0.0060), Chkb (F[2, 6] = 18.22, P = 0.0028), Tekt4 (F[2, 6] = 9.661, P = 0.0133), and Abcb6 (F[2, 6] = 3.840, P = 0.0844) in mice with PSNL-induced neuropathic pain demonstrated that AP treatment significantly decreased the mRNA expression levels in the PFC (Nr4a1, P < 0.001; Rasgrp1, P < 0.01; Rassf1, P < 0.01; Chkb, P < 0.01; Tekt4, P < 0.01; Abcb6, P < 0.01 vs PSNL; Figs. |
| 32796318 |
56289 |
Rassf1
|
Analgesia |
These results suggest that acupuncture can relieve chronic pain-induced comorbid conditions by altering DNA methylation of Nr4a1, Rasgrp1, Rassf1, and Chkb in the PFC. |
| 32796318 |
56289 |
Rassf1
|
Analgesia |
One-way ANOVA with the Newman-Keuls post hoc test for Nr4a1 (F[2, 6] = 28.15, P = 0.0009), Rasgrp1 (F[2, 6] = 21.31, P = 0.0019), Rassf1 (F[2, 6] = 13.52, P = 0.0060), Chkb (F[2, 6] = 18.22, P = 0.0028), Tekt4 (F[2, 6] = 9.661, P = 0.0133), and Abcb6 (F[2, 6] = 3.840, P = 0.0844) in mice with PSNL-induced neuropathic pain demonstrated that AP treatment significantly decreased the mRNA expression levels in the PFC (Nr4a1, P < 0.001; Rasgrp1, P < 0.01; Rassf1, P < 0.01; Chkb, P < 0.01; Tekt4, P < 0.01; Abcb6, P < 0.01 vs PSNL; Figs. |
| 32796318 |
71840 |
Tekt4
|
Analgesia |
One-way ANOVA with the Newman-Keuls post hoc test for Nr4a1 (F[2, 6] = 28.15, P = 0.0009), Rasgrp1 (F[2, 6] = 21.31, P = 0.0019), Rassf1 (F[2, 6] = 13.52, P = 0.0060), Chkb (F[2, 6] = 18.22, P = 0.0028), Tekt4 (F[2, 6] = 9.661, P = 0.0133), and Abcb6 (F[2, 6] = 3.840, P = 0.0844) in mice with PSNL-induced neuropathic pain demonstrated that AP treatment significantly decreased the mRNA expression levels in the PFC (Nr4a1, P < 0.001; Rasgrp1, P < 0.01; Rassf1, P < 0.01; Chkb, P < 0.01; Tekt4, P < 0.01; Abcb6, P < 0.01 vs PSNL; Figs. |
| 34562596 |
11450 |
Adipoq
|
Analgesia |
The deletion of APN significantly reduced the acupuncture analgesia in the CFA-treated APN KO mice while the intrathecal administration of APN mimicked the analgesic effects of EA. |
| 35138669 |
56318 |
Acp3
|
Analgesia |
We hypothesised that EA alleviates pain by inhibiting degradation of the ecto-nucleotidase prostatic acid phosphatase (PAP) and facilitating ATP dephosphorylation in dorsal root ganglions (DRGs). |
| 35138669 |
56318 |
Acp3
|
Analgesia |
CONCLUSIONS: EA treatment alleviated peripheral nerve injury-induced mechanical pain hypersensitivity in mice by inhibiting membrane PAP degradation via reduced endocytosis and subsequently promote ATP dephosphorylation in DRGs. |
| 35656078 |
193034 |
Trpv1
|
Analgesia |
Acupuncture points injection mitigates chronic pain through transient receptor potential V1 in mice |
| 35656078 |
193034 |
Trpv1
|
Analgesia |
These findings suggest that AI can alleviate chronic pain by reducing TRPV1 overexpression in both neuronal and microglial cells. |
| 35656078 |
193034 |
Trpv1
|
Analgesia |
To examine the involvement of TRPV1 channels and related signaling factors in hyperalgesia and AI-mediated analgesia, changes in expression were examined by western blotting of DRG and SC tissue samples isolated after successful induction of hyperalgesia by CIP after reversal by AI (as confirmed by von Fey and Hargreaves' tests). |
| 37519181 |
193034 |
Trpv1
|
Analgesia |
Acupoint Catgut Embedding Diminishes Fibromyalgia Pain through TRPV1 in the Mouse Brain. |
| 37519181 |
193034 |
Trpv1
|
Analgesia |
We aim to determine the properties of acupoint catgut embedding (ACE) on cold stress-induced mice fibromyalgia (FM) and surveyed the character of TRPV1 and linked molecules in chronic FM pain. |
| 37519181 |
193034 |
Trpv1
|
Analgesia |
After ICS, prolonged mechanical and thermal pain was initiated (mechanical threshold: 1.96 +- 0.12 g; thermal latency: 4.86 +- 0.21 s) and were alleviated by ACE treatment and TRPV1 gene deletion. |
| 37519181 |
193034 |
Trpv1
|
Analgesia |
CONCLUSIONS: These novel findings suggest that chronic FM pain can be modulated by ACE or TRPV1 gene deletion. |
| 38164490 |
193034 |
Trpv1
|
Analgesia |
Chronic extensive pain is the main syndrome upsetting individuals with fibromyalgia (FM), accompanied by anxiety, obesity, sleep disturbances, and depression, Transient receptor potential vanilloid 1 (TRPV1) has been reported to transduce inflammatory and pain signals to the brain. |
| 38164490 |
193034 |
Trpv1
|
Analgesia |
Conclusion: We suggest that chronic pain can be modulated by ACE or Trpv1-/-. |
| 38164490 |
193034 |
Trpv1
|
Analgesia |
Acupoint catgut embedding attenuates fibromyalgia pain through attenuation of TRPV1 signaling pathway in mouse. |
| 38164490 |
193034 |
Trpv1
|
Analgesia |
ACE-induced analgesia via TRPV1 signaling pathways may be beneficial targets for FM treatment. |
| 22550540 |
314322 |
Fos
|
Analgesia |
In order to compare the level of c-Fos immunoreactivity in the Formalin group Group 1 with pain-free animals, a normal naive animal group Group 0 was added to this study. |
| 23173601 |
25723 |
Hcrt
|
Analgesia |
Involvement of spinal orexin A in the electroacupuncture analgesia in a rat model of post-laparotomy pain |
| 23173601 |
25593 |
Hcrtr1
|
Analgesia |
The results of the present study indicate the involvement of OXA in EA analgesia via OX1R in an opioid-independent way. |
| 23173601 |
25593 |
Hcrtr1
|
Analgesia |
SB-334867, a selective orexin 1 receptor (OX1R) antagonist with a higher affinity for OXA than OXB, was intrathecally injected to observe its effect on EA analgesia. |
| 23173601 |
25723 |
Hcrt
|
Analgesia |
However, whether OXA is involved in acupuncture analgesia remains unknown. |
| 23173601 |
25723 |
Hcrt
|
Analgesia |
The present study was designed to investigate the involvement of spinal OXA in electroacupuncture (EA) analgesia. |
| 23173601 |
25723 |
Hcrt
|
Analgesia |
SB-334867, a selective orexin 1 receptor (OX1R) antagonist with a higher affinity for OXA than OXB, was intrathecally injected to observe its effect on EA analgesia. |
| 23173601 |
25723 |
Hcrt
|
Analgesia |
Pre-surgical intrathecal administered of SB-334867 30 nmol antagonized OXA analgesia and attenuated the analgesic effect of EA (P<0.05). |
| 23173601 |
25723 |
Hcrt
|
Analgesia |
In addition, naloxone, a selective opioid receptor antagonist, failed to antagonize OXA-induced analgesia (P>0.05). |
| 23173601 |
25723 |
Hcrt
|
Analgesia |
The results of the present study indicate the involvement of OXA in EA analgesia via OX1R in an opioid-independent way. |
| 23173601 |
25723 |
Hcrt
|
Analgesia |
Effect of postoperative OXA injection in the rat model of post-laparotomy pain |
| 23173601 |
25723 |
Hcrt
|
Analgesia |
Effect of preoperative intrathecal injection of SB-334867 on OXA analgesia in the rat model of post-laparotomy pain |
| 23173601 |
25723 |
Hcrt
|
Analgesia |
Effect of pre-treatment with naloxone on OXA analgesia and pre-treatment with SB-334867 on fentanyl-induced analgesia |
| 23573158 |
29256 |
Oprl1
|
Analgesia |
WM significantly reinforced the upregulation of spinal dynorphin mRNA/protein and kappa receptor mRNA levels in CVH rats; (3) intrathecal administration of orphanin-FQ receptor antagonist prior to WM significantly attenuated the WM analgesia and orphanin-FQ enhanced the WM analgesia. |
| 23573158 |
29256 |
Oprl1
|
Analgesia |
WM significantly reinforced the upregulation of spinal dynorphin mRNA/protein and kappa receptor mRNA levels in CVH rats; (3) intrathecal administration of orphanin-FQ receptor antagonist prior to WM significantly attenuated the WM analgesia and orphanin-FQ enhanced the WM analgesia. |
| 24980520 |
78975 |
Prkaa2
|
Analgesia |
Expression levels of the hypothalamic AMPK gene determines the responsiveness of the rats to electroacupuncture-induced analgesia |
| 24980520 |
78975 |
Prkaa2
|
Analgesia |
Our functional genomic study using cDNA microarray identified that 5'-AMP-activated protein kinase (AMPK), a well-known factor in the regulation of energy homeostasis, is the most highly expressed gene in the hypothalamus of the rats that were sensitive to EA analgesia (responder), as compared to the rats that were insensitive to EA analgesia (non-responder). |
| 24980520 |
78975 |
Prkaa2
|
Analgesia |
In this study, we investigated the causal relationship between the hypothalamic AMPK and the individual variation in EA analgesia. |
| 24980520 |
78975 |
Prkaa2
|
Analgesia |
Further, we examined whether viral manipulation of the AMPK expression in the hypothalamus modulates EA analgesia in rats. |
| 24980520 |
78975 |
Prkaa2
|
Analgesia |
Microinjection of dominant negative (DN) AMPK adenovirus, which inhibits AMPK activity, into the rat hypothalamus significantly attenuates EA analgesia (p < 0.05), whereas wild type (WT) AMPK virus did not affect EA analgesia (p > 0.05). |
| 24980520 |
78975 |
Prkaa2
|
Analgesia |
The present results demonstrated that levels of AMPK gene expression in the rat hypothalamus determine the individual differences in the sensitivity to EA analgesia. |
| 24980520 |
78975 |
Prkaa2
|
Analgesia |
Effects of adenoviral gene transfer of AMPK into the hypothalamus on EA-induced analgesia |
| 25074385 |
25712 |
Ifng
|
Analgesia |
Since excessive release of interferon-gamma (IFN-gamma) after nerve injury transforms quiescent spinal microglia into an activated state with more neuropathic pain, associated with purinergic receptor P2X4 expression, it is possible that EA may mediate its analgesic effect by attenuating IFN-gamma release and subsequent generation of P2X4R(+) microglia. |
| 25074385 |
25712 |
Ifng
|
Analgesia |
METHODS: Male rats underwent chronic constriction injury (CCI) or IFN-gamma intrathecal injection and von Frey tests were performed to evaluate the effect of EA on pain thresholds. |
| 25074385 |
25712 |
Ifng
|
Analgesia |
Electroacupuncture inhibits excessive interferon-gamma evoked up-regulation of P2X4 receptor in spinal microglia in a CCI rat model for neuropathic pain. |
| 25158599 |
25712 |
Ifng
|
Analgesia |
Repeated EA interventions have a time-dependent cumulative analgesic effect in neuropathic pain rats, which is closely associated with its regulatory effects on NK cells, splenic IL-2, beta-EP, and plasma IL-2, IL-1beta, IFN-gamma and TGF-beta levels. |
| 25158599 |
24494 |
Il1b
|
Analgesia |
Repeated EA interventions have a time-dependent cumulative analgesic effect in neuropathic pain rats, which is closely associated with its regulatory effects on NK cells, splenic IL-2, beta-EP, and plasma IL-2, IL-1beta, IFN-gamma and TGF-beta levels. |
| 25158599 |
116562 |
Il2
|
Analgesia |
Repeated EA interventions have a time-dependent cumulative analgesic effect in neuropathic pain rats, which is closely associated with its regulatory effects on NK cells, splenic IL-2, beta-EP, and plasma IL-2, IL-1beta, IFN-gamma and TGF-beta levels. |
| 25158599 |
59086 |
Tgfb1
|
Analgesia |
Repeated EA interventions have a time-dependent cumulative analgesic effect in neuropathic pain rats, which is closely associated with its regulatory effects on NK cells, splenic IL-2, beta-EP, and plasma IL-2, IL-1beta, IFN-gamma and TGF-beta levels. |
| 25206545 |
287989 |
Ephb3
|
Analgesia |
Electroacupuncture signifi-cantly enhanced the mRNA expression of ephrin-B3 and EphB3/B6 in the dorsal horns of neuro-pathic pain rats. |
| 25206545 |
360546 |
Efnb3
|
Analgesia |
Electroacupuncture signifi-cantly enhanced the mRNA expression of ephrin-B3 and EphB3/B6 in the dorsal horns of neuro-pathic pain rats. |
| 25368638 |
81739 |
P2rx3
|
Analgesia |
In neuropathic pain, there is upregulation of P2X purinoceptor 3 (P2X3) receptor expression in dorsal root ganglion neurons. |
| 25368638 |
81739 |
P2rx3
|
Analgesia |
Electroacupuncture may act via purinergic A1 and P2X3 receptors simultaneously to induce an analgesic effect on neuropathic pain. |
| 25657670 |
54232 |
Car3
|
Analgesia |
Repeated electroacupuncture intervention had a cumulative analgesic effect on injury-induced neuropathic pain reactions, and it led to synaptic remodeling of hippocampal neurons and upregulated calcium/calmodulin-dependent protein kinase II expression in the hippocampal CA3 region. |
| 25767502 |
83817 |
Ache
|
Analgesia |
Results demonstrated increased expression of hippocampal acetylcholinesterase, vesicular acetylcholine transporter, and muscarinic M1 receptor mRNA, as well as decreased pain threshold, in a rat model of chronic neuropathic pain after electroacupuncture. |
| 25767502 |
60422 |
Slc18a3
|
Analgesia |
The present study observed the effects of repeated electroacupuncture of Zusanli (ST36) and Yanglingquan (GB34) on expression of hippocampal acetylcholinesterase, vesicular acetylcholine transporter, and muscarinic M1 receptor mRNA in chronic constrictive injury (neuropathic pain) and/or ovariotomy rats. |
| 25767502 |
83817 |
Ache
|
Analgesia |
The present study observed the effects of repeated electroacupuncture of Zusanli (ST36) and Yanglingquan (GB34) on expression of hippocampal acetylcholinesterase, vesicular acetylcholine transporter, and muscarinic M1 receptor mRNA in chronic constrictive injury (neuropathic pain) and/or ovariotomy rats. |
| 25767502 |
60422 |
Slc18a3
|
Analgesia |
The present study observed the effects of repeated electroacupuncture of Zusanli (ST36) and Yanglingquan (GB34) on expression of hippocampal acetylcholinesterase, vesicular acetylcholine transporter, and muscarinic M1 receptor mRNA in chronic constrictive injury (neuropathic pain) and/or ovariotomy rats. |
| 26064176 |
25238 |
Grk2
|
Analgesia |
The attenuation of G protein-coupled receptor kinase 2 (GRK2) in spinal cord and peripheral nociceptor has been widely acknowledged to promote the transition from acute to chronic pain and to facilitate the nociceptive progress. |
| 26064176 |
25238 |
Grk2
|
Analgesia |
This study was designed to investigate the possible role of spinal GRK2 in EA antiallodynic in a rat model with complete Freund's adjuvant (CFA) induced inflammatory pain. |
| 26064176 |
25238 |
Grk2
|
Analgesia |
These pieces of data demonstrated that the spinal GRK2 played an important role in EA antiallodynia on inflammatory pain. |
| 26184310 |
24387 |
Gfap
|
Analgesia |
Repetitive saline injection during the induction phase significantly increased GFAP expression in the spinal dorsal horn compared with that of normal animals (** p < 0.01), and repetitive DBV treatment at ST36 suppressed SCI-enhanced GFAP expression (# p < 0.05), suggesting that DBV treatment has a potent anti-nociceptive effect on SCI-induced central neuropathic pain. |
| 26338695 |
108348108 |
Hspa1b
|
Analgesia |
CONCLUSIONS: The up-regulation of TRPV1 and HSP70 expression in bone marrow cells may be involved in visceral pain development and the analgesic effect of moxibustion on VH may be mediated through down-regulation of TRPV1 and HSP70 expression in bone marrow cells. |
| 26338695 |
83810 |
Trpv1
|
Analgesia |
CONCLUSIONS: The up-regulation of TRPV1 and HSP70 expression in bone marrow cells may be involved in visceral pain development and the analgesic effect of moxibustion on VH may be mediated through down-regulation of TRPV1 and HSP70 expression in bone marrow cells. |
| 26770252 |
50689 |
Mapk3
|
Analgesia |
Strong Manual Acupuncture Stimulation of Huantiao (GB 30) Reduces Pain-Induced Anxiety and p-ERK in the Anterior Cingulate Cortex in a Rat Model of Neuropathic Pain |
| 26770252 |
116590 |
Mapk1
|
Analgesia |
Strong Manual Acupuncture Stimulation of Huantiao (GB 30) Reduces Pain-Induced Anxiety and p-ERK in the Anterior Cingulate Cortex in a Rat Model of Neuropathic Pain |
| 26770252 |
50689 |
Mapk3
|
Analgesia |
The phosphorylation of extracellular signal-regulated kinase (p-ERK) in the anterior cingulate cortex (ACC) plays an important role in pain-induced anxiety. |
| 26770252 |
116590 |
Mapk1
|
Analgesia |
The phosphorylation of extracellular signal-regulated kinase (p-ERK) in the anterior cingulate cortex (ACC) plays an important role in pain-induced anxiety. |
| 26770252 |
50689 |
Mapk3
|
Analgesia |
However, little is known about which acupuncture technique is optimal on pain-induced anxiety and the relationship between acupuncture effect and p-ERK. |
| 26770252 |
116590 |
Mapk1
|
Analgesia |
However, little is known about which acupuncture technique is optimal on pain-induced anxiety and the relationship between acupuncture effect and p-ERK. |
| 26770252 |
50689 |
Mapk3
|
Analgesia |
The pain withdrawal thresholds (PWTs) and anxiety behavior were measured, and p-ERK protein expression and immunoreactivity cells in ACC were detected. |
| 26770252 |
116590 |
Mapk1
|
Analgesia |
The pain withdrawal thresholds (PWTs) and anxiety behavior were measured, and p-ERK protein expression and immunoreactivity cells in ACC were detected. |
| 26770252 |
50689 |
Mapk3
|
Analgesia |
The effect of different acupuncture techniques on pain-induced anxiety may arise from the regulation of p-ERK in ACC. |
| 26770252 |
116590 |
Mapk1
|
Analgesia |
The effect of different acupuncture techniques on pain-induced anxiety may arise from the regulation of p-ERK in ACC. |
| 26896072 |
314322 |
Fos
|
Analgesia |
Preemptive Analgesia with Acupuncture Monitored by c-Fos Expression in Rats. |
| 26896072 |
314322 |
Fos
|
Analgesia |
In the control rats, c-fos expression was higher before surgery than after surgery, contradicting the expected outcome of acupuncture and preemptive analgesia. |
| 27301303 |
24473 |
Htr1a
|
Analgesia |
Serotonin (5-HT), as a representative substance released by mast cells, plays a pivotal role in alleviating pain. |
| 27411565 |
79246 |
Htr3a
|
Analgesia |
The 5-HT3 receptor Involvement of EA-induced analgesia |
| 27411565 |
79246 |
Htr3a
|
Analgesia |
The effects of the 5-HT3 receptor agonist mCLBG and antagonist ODSTN on the analgesia induced by 2 Hz EA in the CIOA rat model are shown in Fig. |
| 27978835 |
170851 |
Map2k1
|
Analgesia |
Activation of hippocampal MEK1 contributes to the cumulative antinociceptive effect of electroacupuncture in neuropathic pain rats |
| 27978835 |
170851 |
Map2k1
|
Analgesia |
Therefore, the present study investigated the relationship between the effects of different numbers of EA intervention sessions and the activation of MEK1 in the hippocampus and hypothalamus in a rat model of neuropathic pain. |
| 27978835 |
170851 |
Map2k1
|
Analgesia |
EA intervention can induce time-dependent cumulative analgesia in neuropathic pain rats after 4 successive sessions of daily EA intervention, which is at least in part related to the activation of hippocampal MEK1. |
| 28600329 |
24241 |
Calca
|
Analgesia |
The aim of this study was to investigate whether expression of gamma-aminobutyric acid (GABA) and the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) in the primary sensory neurons of cervical dorsal root ganglia (DRG) are involved in electroacupuncture (EA)-induced analgesia in a rat model of incisional neck pain. |
| 28600329 |
24241 |
Calca
|
Analgesia |
EA at LI18/LI4-PC6 increases PT in rats with incisional neck pain, which is likely related to downregulation of pronociceptive mediators SP/CGRP and upregulation of the inhibitory transmitter GABA in the primary sensory neurons of cervical DRGs. |
| 29034548 |
24473 |
Htr1a
|
Analgesia |
To investigate the roles of 5-HT1A receptors in the effect of EA on paclitaxel-induced pain, rats were injected with paclitaxel and divided into four groups (n=7 per group): 1) WAY-100635 (12.5 nmol / 5 mul, a 5-HT 1A receptor antagonist) + EA, 2) WAY-100635 + sham, 3) saline + EA, and 4) saline + sham. |
| 29034548 |
24473 |
Htr1a
|
Analgesia |
As aforementioned in introduction, it is not known whether 5-HT1A receptors are involved in EA inhibition of neuropathic pain. |
| 29034548 |
24473 |
Htr1a
|
Analgesia |
To investigate the roles of 5-HT1A receptors in the effect of EA on paclitaxel-induced pain, rats were injected with paclitaxel and divided into four groups (n=7 per group): 1) WAY-100635 (12.5 nmol / 5 mul, a 5-HT 1A receptor antagonist) + EA, 2) WAY-100635 + sham, 3) saline + EA, and 4) saline + sham. |
| 29034548 |
25400 |
Camk2a
|
Analgesia |
Electroacupuncture alleviates chemotherapy-induced pain through inhibiting phosphorylation of spinal CaMKII in rats |
| 29034548 |
25400 |
Camk2a
|
Analgesia |
This indicates that KN-93 may inhibit pain through suppressing the p-CaMKII. |
| 29436370 |
310738 |
Ngf
|
Analgesia |
There was an interaction between the independent variables: pain, treatments, and anesthesia in serum S100beta levels and NGF levels in the left sciatic nerve. |
| 27707699 |
25601 |
Oprm1
|
Analgesia |
The aim of the present study was to observe the effects of different frequencies of TEAS on pain measures and expression of mu opioid receptors (MORs) in the dorsal root ganglion (DRG) of rats |
| 27707699 |
25601 |
Oprm1
|
Analgesia |
The aim of the present study was to observe the effects of different frequencies of TEAS on pain measures and expression of mu opioid receptors (MORs) in the dorsal root ganglion (DRG) of rats |
| 27843474 |
24473 |
Htr1a
|
Analgesia |
Radioimmunoassay and high-performance liquid chromatography were used to evaluate the expression of 5-hydroxytryptamine (HT) in the plasma and three-key structure of the descending pain modulatory system. |
| 27843474 |
24473 |
Htr1a
|
Analgesia |
Furthermore, we found that the level of 5-HT in plasma was significantly increased, and it was significantly decreased in the descending pain modulatory system in Model group. |
| 28672900 |
24473 |
Htr1a
|
Analgesia |
100-Hz EA alleviated the pain-depression dyad and upregulated 5-HT in the DRN of reserpine-injected rats. |
| 28672900 |
24473 |
Htr1a
|
Analgesia |
The present study was the first to demonstrate that 5-HT in the DRN is involved in mediating the analgesic and anti-depressive effects of 100-Hz EA on the pain-depression dyad. |
| 28672900 |
24473 |
Htr1a
|
Analgesia |
HPLC-ECD was adopted to determine the effect of 100-Hz EA on 5-HT levels in the DRN in rats with pain-depression dyad. |
| 34472492 |
25601 |
Oprm1
|
Analgesia |
The results revealed that electroacupuncture treatment increased the mechanical response threshold of hind paw of nicotine-dependent rats with hyperalgesia and up-regulated the protein expression of pain-related factors mu-opioid receptor, beta-endorphin and glutamic acid decarboxylase 65 in the spinal cord and midbrain periaqueductal gray and the protein expression of glutamic acid decarboxylase 67 in the spinal cord. |
| 34472492 |
24380 |
Gad2
|
Analgesia |
The results revealed that electroacupuncture treatment increased the mechanical response threshold of hind paw of nicotine-dependent rats with hyperalgesia and up-regulated the protein expression of pain-related factors mu-opioid receptor, beta-endorphin and glutamic acid decarboxylase 65 in the spinal cord and midbrain periaqueductal gray and the protein expression of glutamic acid decarboxylase 67 in the spinal cord. |
| 34472492 |
24379 |
Gad1
|
Analgesia |
The results revealed that electroacupuncture treatment increased the mechanical response threshold of hind paw of nicotine-dependent rats with hyperalgesia and up-regulated the protein expression of pain-related factors mu-opioid receptor, beta-endorphin and glutamic acid decarboxylase 65 in the spinal cord and midbrain periaqueductal gray and the protein expression of glutamic acid decarboxylase 67 in the spinal cord. |
| 31217804 |
314322 |
Fos
|
Analgesia |
C-Fos expression is regarded as a biomarker of pain-related behavior, reflecting the degree of hyperalgesia and the level of activation of the trigeminovascular system (TS). |
| 37143500 |
25248 |
Cnr1
|
Analgesia |
Figure 3A shows Western blotting results revealing the effect of each treatment on the expression of pain-related proteins, including c-Fos, CB1R, FAAH, NeuN, synapsin I, and MAP2. |
| 37143500 |
314322 |
Fos
|
Analgesia |
Figure 3A shows Western blotting results revealing the effect of each treatment on the expression of pain-related proteins, including c-Fos, CB1R, FAAH, NeuN, synapsin I, and MAP2. |
| 37143500 |
100911581 |
Faah
|
Analgesia |
Figure 3A shows Western blotting results revealing the effect of each treatment on the expression of pain-related proteins, including c-Fos, CB1R, FAAH, NeuN, synapsin I, and MAP2. |
| 37143500 |
25595 |
Map2
|
Analgesia |
Figure 3A shows Western blotting results revealing the effect of each treatment on the expression of pain-related proteins, including c-Fos, CB1R, FAAH, NeuN, synapsin I, and MAP2. |
| 37143500 |
287847 |
Rbfox3
|
Analgesia |
Figure 3A shows Western blotting results revealing the effect of each treatment on the expression of pain-related proteins, including c-Fos, CB1R, FAAH, NeuN, synapsin I, and MAP2. |
| 37143500 |
24949 |
Syn1
|
Analgesia |
Figure 3A shows Western blotting results revealing the effect of each treatment on the expression of pain-related proteins, including c-Fos, CB1R, FAAH, NeuN, synapsin I, and MAP2. |
| 32042305 |
79246 |
Htr3a
|
Analgesia |
WAA, similar to EA, alleviated mechanical hyperalgesia in CIBP rats by suppressing the expressions of 5-HT and 5-HT3AR, and increasing the expressions of MOR and endomorphin-1 in RVM-spinal cord pathway of the descending pain-modulating system. |
| 32042305 |
25601 |
Oprm1
|
Analgesia |
WAA, similar to EA, alleviated mechanical hyperalgesia in CIBP rats by suppressing the expressions of 5-HT and 5-HT3AR, and increasing the expressions of MOR and endomorphin-1 in RVM-spinal cord pathway of the descending pain-modulating system. |
| 31775332 |
301059 |
Myd88
|
Analgesia |
TLR4 and its downstream signaling molecule MyD88 are both increased in DRGs of paclitaxel-treated rats and are involved in paclitaxel-induced peripheral neuropathic pain. |
| 31775332 |
29260 |
Tlr4
|
Analgesia |
TLR4 and its downstream signaling molecule MyD88 are both increased in DRGs of paclitaxel-treated rats and are involved in paclitaxel-induced peripheral neuropathic pain. |
| 31775332 |
29260 |
Tlr4
|
Analgesia |
Electroacupuncture Alleviates Paclitaxel-Induced Peripheral Neuropathic Pain in Rats via Suppressing TLR4 Signaling and TRPV1 Upregulation in Sensory Neurons |
| 31775332 |
29260 |
Tlr4
|
Analgesia |
These results demonstrated that EA alleviates paclitaxel-induced peripheral neuropathic pain via mechanisms possibly involving suppressing TLR4 signaling and TRPV1 upregulation in DRG neurons, which further result in reduced spinal glia activation. |
| 31775332 |
83810 |
Trpv1
|
Analgesia |
Electroacupuncture Alleviates Paclitaxel-Induced Peripheral Neuropathic Pain in Rats via Suppressing TLR4 Signaling and TRPV1 Upregulation in Sensory Neurons |
| 31775332 |
83810 |
Trpv1
|
Analgesia |
Pharmacological blocking of TRPV1 mimics the analgesic effects of EA on the pain hypersensitivities, whereas capsaicin reversed EA's effect. |
| 31775332 |
83810 |
Trpv1
|
Analgesia |
These results demonstrated that EA alleviates paclitaxel-induced peripheral neuropathic pain via mechanisms possibly involving suppressing TLR4 signaling and TRPV1 upregulation in DRG neurons, which further result in reduced spinal glia activation. |
| 31775332 |
83810 |
Trpv1
|
Analgesia |
It is well established that TRPV1 channel expression is increased in DRGs upon paclitaxel treatment and plays a critical role in mediating paclitaxel-induced peripheral neuropathic pain. |
| 31775332 |
83810 |
Trpv1
|
Analgesia |
Pharmacological Blocking of TRPV1 Mimics EA's Therapeutic Effect in Reducing Pain Hypersensitivities of Paclitaxel-Treated Rats |
| 31775332 |
83810 |
Trpv1
|
Analgesia |
These results further support the notion that EA's analgesic effect on paclitaxel-induced pain hypersensitivities is mediated by TRPV1 modulation. |
| 31775332 |
83810 |
Trpv1
|
Analgesia |
We next examined the effects of AMG9810, the specific TRPV1 antagonist, on the pain hypersensitivities of paclitaxel-treated rats. |
| 33398365 |
29659 |
P2rx4
|
Analgesia |
In order to demonstrate the possibility that EA analgesia is mediated in part by P2X4R in hyperactive microglia, the present study performed mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) tests in male Sprague-Dawley rats that had undergone spinal nerve ligation (SNL). |
| 33398365 |
29659 |
P2rx4
|
Analgesia |
The results of the present study indicate that EA may mediate P2X4R in hyperactive spinal microglia to inhibit nociceptive transmission of SG neurons, thus relieving pain in SNL rats. |
| 35416841 |
29290 |
Adora1
|
Analgesia |
Lastly, the adenosine A1 receptor agonist N6-cyclopentyladenosine was intrathecally injected into the lumbar swelling of the rats, and the mechanical withdrawal and thermal pain thresholds were reevaluated. |
| 35416841 |
58813 |
Nt5e
|
Analgesia |
This study aimed to determine the role that ecto-5'-nucleotidase plays in EA-induced analgesia for neuropathic pain. |
| 35416841 |
58813 |
Nt5e
|
Analgesia |
We observed the mechanical withdrawal threshold and thermal pain threshold and detected the expression of ecto-5'-nucleotidase in the spinal cord using Western blot. |
| 35416841 |
58813 |
Nt5e
|
Analgesia |
Analgesia and increased ecto-5'-nucleotidase expression and adenosine content in the spinal cord were observed 1 h after electroacupuncture. |
| 35416841 |
58813 |
Nt5e
|
Analgesia |
Our results suggest that electroacupuncture at Zusanli can produce analgesia in chronic constriction injury rat models, possibly via the increased ecto-5'-nucleotidase expression induced through electroacupuncture, thus leading to increased adenosine expression in the spinal cord. |
| 35100811 |
54250 |
Fgf2
|
Analgesia |
Electroacupuncture suppresses spinal nerve ligation-induced neuropathic pain via regulation of synaptic plasticity through upregulation of basic fibroblast growth factor expression. |
| 35100811 |
54250 |
Fgf2
|
Analgesia |
CONCLUSION: These findings indicate that EA suppresses SNL-induced neuropathic pain by improving synaptic plasticity via upregulation of bFGF expression. |
| 31737064 |
58959 |
Crhr1
|
Analgesia |
Compared with the blank control group, visceral pain threshold pressure, the expression of ZO-1, OT%, SP%, CRF, and CRF-R1 mRNA expression in the hypothalamus, and double staining of IMMC and CRF-R1 were decreased significantly in the CUMS group. |
| 31737064 |
292994 |
Tjp1
|
Analgesia |
Compared with the blank control group, visceral pain threshold pressure, the expression of ZO-1, OT%, SP%, CRF, and CRF-R1 mRNA expression in the hypothalamus, and double staining of IMMC and CRF-R1 were decreased significantly in the CUMS group. |
| 38026466 |
24770 |
Ccl2
|
Analgesia |
Conclusion: IQAB reduced p38-activation-related microglia activation and MCP-1 levels, thus alleviating pathological changes, inflammation levels in the local spinal cord, and pain behavior of CSR. |
| 38026466 |
81649 |
Mapk14
|
Analgesia |
Conclusion: IQAB reduced p38-activation-related microglia activation and MCP-1 levels, thus alleviating pathological changes, inflammation levels in the local spinal cord, and pain behavior of CSR. |
| 37548586 |
24225 |
Bdnf
|
Analgesia |
EA improved pain threshold and motor function in CSR rats, inhibited the expression of BDNF, P-TrkB, CAMKII, and P-CREB in spinal cord synapses, reduced the expression of pain factor c-fos and postsynaptic membrane protein molecule neuroligin2, exerted a modulating effect on spinal cord synaptic plasticity in CSR rats, and suppressed the overactive synaptic efficacy. |
| 37548586 |
24245 |
Camk2b
|
Analgesia |
EA improved pain threshold and motor function in CSR rats, inhibited the expression of BDNF, P-TrkB, CAMKII, and P-CREB in spinal cord synapses, reduced the expression of pain factor c-fos and postsynaptic membrane protein molecule neuroligin2, exerted a modulating effect on spinal cord synaptic plasticity in CSR rats, and suppressed the overactive synaptic efficacy. |
| 37548586 |
24245 |
Camk2b
|
Analgesia |
Electroacupuncture ameliorates pain in cervical spondylotic radiculopathy rat by inhibiting the CaMKII/CREB/BDNF signaling pathway and regulating spinal synaptic plasticity |
| 37548586 |
24225 |
Bdnf
|
Analgesia |
Electroacupuncture ameliorates pain in cervical spondylotic radiculopathy rat by inhibiting the CaMKII/CREB/BDNF signaling pathway and regulating spinal synaptic plasticity |
| 37548586 |
81646 |
Creb1
|
Analgesia |
Electroacupuncture ameliorates pain in cervical spondylotic radiculopathy rat by inhibiting the CaMKII/CREB/BDNF signaling pathway and regulating spinal synaptic plasticity |
| 37548586 |
314322 |
Fos
|
Analgesia |
EA improved pain threshold and motor function in CSR rats, inhibited the expression of BDNF, P-TrkB, CAMKII, and P-CREB in spinal cord synapses, reduced the expression of pain factor c-fos and postsynaptic membrane protein molecule neuroligin2, exerted a modulating effect on spinal cord synaptic plasticity in CSR rats, and suppressed the overactive synaptic efficacy. |
| 37548586 |
314322 |
Fos
|
Analgesia |
The above suggests that EA can inhibit the expression of c-fos, the pain target gene of CRE sequence promoter, and inhibit the excitation of spinal cord synaptic neurons, which in turn has an analgesic effect. |
| 37548586 |
81646 |
Creb1
|
Analgesia |
EA improved pain threshold and motor function in CSR rats, inhibited the expression of BDNF, P-TrkB, CAMKII, and P-CREB in spinal cord synapses, reduced the expression of pain factor c-fos and postsynaptic membrane protein molecule neuroligin2, exerted a modulating effect on spinal cord synaptic plasticity in CSR rats, and suppressed the overactive synaptic efficacy. |
| 37548586 |
117096 |
Nlgn2
|
Analgesia |
EA improved pain threshold and motor function in CSR rats, inhibited the expression of BDNF, P-TrkB, CAMKII, and P-CREB in spinal cord synapses, reduced the expression of pain factor c-fos and postsynaptic membrane protein molecule neuroligin2, exerted a modulating effect on spinal cord synaptic plasticity in CSR rats, and suppressed the overactive synaptic efficacy. |
| 37548586 |
25054 |
Ntrk2
|
Analgesia |
EA improved pain threshold and motor function in CSR rats, inhibited the expression of BDNF, P-TrkB, CAMKII, and P-CREB in spinal cord synapses, reduced the expression of pain factor c-fos and postsynaptic membrane protein molecule neuroligin2, exerted a modulating effect on spinal cord synaptic plasticity in CSR rats, and suppressed the overactive synaptic efficacy. |
| 35069759 |
29397 |
Ccl11
|
Analgesia |
Furthermore, we found that the effects of TN against CCD-induced menstrual pain, increased ECP expression, and HIS level were abolished by CCL11. |
| 35069759 |
29397 |
Ccl11
|
Analgesia |
To further address whether pain-relief induced by TN was dependent on the activation of the eotaxin/CCR3 axis, we injected CCR3 antagonist SB328437 and agonist CCL11. |
| 35069759 |
29397 |
Ccl11
|
Analgesia |
However, after the application of CCL11 in the TN group, it markedly weakened TN-induced pain relief compared with the Model + Vehicle2 + TN group as manifested by the number of contraction wave, uterine peak-to-peak value, and degree of contraction (P < 0.01, P < 0.05; Figures 7(b)-7(d)). |
| 35069759 |
117027 |
Ccr3
|
Analgesia |
The purpose of this study is to investigate whether eotaxin/CC chemokine receptor 3 (CCR3) axis, a key regulatory pathway for eosinophils (EOS) recruitment, is involved in acupuncture analgesia for dysmenorrhea. |
| 35069759 |
117027 |
Ccr3
|
Analgesia |
Acupuncture Alleviates Menstrual Pain in Rat Model via Suppressing Eotaxin/CCR3 Axis to Weak EOS-MC Activation |
| 35069759 |
117027 |
Ccr3
|
Analgesia |
The purpose of this study is to investigate whether eotaxin/CC chemokine receptor 3 (CCR3) axis, a key regulatory pathway for eosinophils (EOS) recruitment, is involved in acupuncture analgesia for dysmenorrhea. |
| 35069759 |
117027 |
Ccr3
|
Analgesia |
TN alleviated menstrual pain by improving the uterine inflammatory environment via suppressing eotaxin/CCR3 axis to weak EOS-MC activation in CCD rats. |
| 35069759 |
117027 |
Ccr3
|
Analgesia |
TN at SP6 can relieve pain by attenuating the expression of eotaxin/CCR3 axis and EOS-MC activation. |
| 35069759 |
117027 |
Ccr3
|
Analgesia |
To further address whether pain-relief induced by TN was dependent on the activation of the eotaxin/CCR3 axis, we injected CCR3 antagonist SB328437 and agonist CCL11. |
| 35069759 |
29397 |
Ccl11
|
Analgesia |
Acupuncture Alleviates Menstrual Pain in Rat Model via Suppressing Eotaxin/CCR3 Axis to Weak EOS-MC Activation |
| 35069759 |
29397 |
Ccl11
|
Analgesia |
The purpose of this study is to investigate whether eotaxin/CC chemokine receptor 3 (CCR3) axis, a key regulatory pathway for eosinophils (EOS) recruitment, is involved in acupuncture analgesia for dysmenorrhea. |
| 35069759 |
29397 |
Ccl11
|
Analgesia |
TN alleviated menstrual pain by improving the uterine inflammatory environment via suppressing eotaxin/CCR3 axis to weak EOS-MC activation in CCD rats. |
| 35069759 |
29397 |
Ccl11
|
Analgesia |
TN at SP6 can relieve pain by attenuating the expression of eotaxin/CCR3 axis and EOS-MC activation. |
| 35069759 |
117027 |
Ccr3
|
Analgesia |
To further address whether pain-relief induced by TN was dependent on the activation of the eotaxin/CCR3 axis, we injected CCR3 antagonist SB328437 and agonist CCL11. |
| 35069759 |
29397 |
Ccl11
|
Analgesia |
To further address whether pain-relief induced by TN was dependent on the activation of the eotaxin/CCR3 axis, we injected CCR3 antagonist SB328437 and agonist CCL11. |
| 35069759 |
|
|
Analgesia |
Furthermore, we found that the effects of TN against CCD-induced menstrual pain, increased ECP expression, and HIS level were abolished by CCL11. |
| 484537 |
100350756 |
OPRM1
|
Analgesia |
The possible role of endorphins in the mechanism of acupuncture analgesia is discussed. |
| 1350448 |
24613 |
Oprd1
|
Analgesia |
The results indicate that 2 Hz-EA analgesia is mediated by mu- and delta-receptors, 100 Hz-EA analgesia by kappa-receptor, and 2-15 Hz-EA analgesia by combined action of mu-, delta- and kappa-receptors in the spinal cord of the rats. |
| 1350448 |
29335 |
Oprk1
|
Analgesia |
The results indicate that 2 Hz-EA analgesia is mediated by mu- and delta-receptors, 100 Hz-EA analgesia by kappa-receptor, and 2-15 Hz-EA analgesia by combined action of mu-, delta- and kappa-receptors in the spinal cord of the rats. |
| 1350448 |
25601 |
Oprm1
|
Analgesia |
The results indicate that 2 Hz-EA analgesia is mediated by mu- and delta-receptors, 100 Hz-EA analgesia by kappa-receptor, and 2-15 Hz-EA analgesia by combined action of mu-, delta- and kappa-receptors in the spinal cord of the rats. |
| 2274271 |
25298 |
Cck
|
Analgesia |
Results suggest that CCK acts as a neurotransmitter in the medial thalamus, a part of the analgesia inhibitory system. |
| 8822091 |
100009275 |
TAC1
|
Analgesia |
effects of EAP on evoked potentials and release of substance P (SP) following tooth pulp stimulation (ST) in the superficial layers of the trigeminal nucleus caudalis (Vc-I-II) were studied in the rabbit.These findings suggested that SP might play an important role in the transmission of pain in the trigeminal afferent nociceptive pathways. |
| 10579240 |
24316 |
Drd1
|
Analgesia |
Previous studies have shown that dopamine (DA) is involved in electroacupuncture analgesia (EAA), a DA receptor antagonist was proved to potentiate EAA in both laboratory research and clinical practice. |
| 10579240 |
24318 |
Drd2
|
Analgesia |
Increasing attention had been paid on the role of N. accumbens in pain modulation(14). There are clear distinctions between D1 and D2 receptors in localizaton and bicchemistry(I5). |
| 15336634 |
25083 |
Adra2a
|
Analgesia |
Acupoint Stimulation With Diluted Bee Venom (Apipuncture) Alleviates Thermal Hyperalgesia in a Rodent Neuropathic Pain Model: Involvement of Spinal Alpha2-Adrenoceptors |
| 15629266 |
24473 |
Htr1a
|
Analgesia |
the influence of 5-HT upon the activity of nocisponsive neurones in the dorsal horn is heterogeneous.In the present study, we have shown that intrathecal administration of the non-selective serotonin receptor blocker methysergide antagonized apipuncture-induced antinociception suggestingthat a serotoninergic spinal cord component is involved in apipuncture analgesia. |
| 16459202 |
24221 |
Avp
|
Analgesia |
pain stimulation could change the AVP concentrations only in the rat brain nuclei, not in spinal cord and blood; only intraventricular injection, not intrathecal injection and intravenous injection, of AVP increased the pain threshold, whereas intraventricular injection, not intrathecal injection and intravenous injection, of anti-AVP serum decreased the pain threshold.acupuncture decreased inter-cell AVP, i.e.AVP immunoreactivecells, not OXT, L-Ek, -Ep and DynA1-13 immunoreactive cells in PVH using immunocytochemistry. |
| 16490194 |
25453 |
Gdnf
|
Analgesia |
An important finding in the present study is that co-application of electroacupuncture with intrathecal injection of a glial metabolic inhibitor fluorocitrate synergistically antagonized rat monoarthritic pain. |
| 17005164 |
24408 |
Grin1
|
Analgesia |
These results suggest that EA affects the progress of experimental inflammatory pain by modulating the expression of NMDA receptors in primary sensory neurons, in particular, IB4-positive small neurons. |
| 19022309 |
24221 |
Avp
|
Analgesia |
Arginine vasopressin (AVP) has been proven to be involved in the process of pain regulation. |
| 19409856 |
25248 |
Cnr1
|
Analgesia |
we determined the effect of electroacupuncture (EA) on the level of anandamide in the skin tissue and the role of cannabinoid CB1 and CB2 receptors in the analgesic effect of EA in an animal model of inflammatory pain. |
| 19409856 |
57302 |
Cnr2
|
Analgesia |
we determined the effect of electroacupuncture (EA) on the level of anandamide in the skin tissue and the role of cannabinoid CB1 and CB2 receptors in the analgesic effect of EA in an animal model of inflammatory pain. |
| 20130880 |
25601 |
Oprm1
|
Analgesia |
The selective antagonist of the mu opioid receptor (OR) signiWcantly suppressed contralateral ST36 EA-induced analgesia against carrageenan-induced inXammation. |
| 20654703 |
29527 |
Ptgs2
|
Analgesia |
Our recent study has shown that it may inhibit cyclooxygenase-2 (COX-2) in the spinal dorsal horn where COX-2 is upregulated after the development of neuropathic pain following spinal nerve ligation (SNL). |
| 21680256 |
24494 |
Il1b
|
Analgesia |
The present study demonstrated that: 1) repeated EA stimulation of ipsilateral GB30 and GB34 acupoints remarkably suppressed CFA-induced hyperalgesia; 2) EA treatment markedly enhanced the upregulation of spinal NT-3 mRNA and protein levels following CFA injection; 3) antisense oligodeoxynucleotides (ODN) specifically against NT-3 intrathecally administered during EA treatment for 7 days significantly attenuated the EA analgesia; and 4) the suppressed expression of spinal GFAP (astrocytic marker), OX-42 (microglial marker) as well as proinflammatory cytokines, interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha by EA treatment was significantly attenuated following NT-3 antisense ODN delivery. |
| 21680256 |
24835 |
Tnf
|
Analgesia |
The present study demonstrated that: 1) repeated EA stimulation of ipsilateral GB30 and GB34 acupoints remarkably suppressed CFA-induced hyperalgesia; 2) EA treatment markedly enhanced the upregulation of spinal NT-3 mRNA and protein levels following CFA injection; 3) antisense oligodeoxynucleotides (ODN) specifically against NT-3 intrathecally administered during EA treatment for 7 days significantly attenuated the EA analgesia; and 4) the suppressed expression of spinal GFAP (astrocytic marker), OX-42 (microglial marker) as well as proinflammatory cytokines, interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha by EA treatment was significantly attenuated following NT-3 antisense ODN delivery. |
| 21680256 |
24387 |
Gfap
|
Analgesia |
The present study demonstrated that: 1) repeated EA stimulation of ipsilateral GB30 and GB34 acupoints remarkably suppressed CFA-induced hyperalgesia; 2) EA treatment markedly enhanced the upregulation of spinal NT-3 mRNA and protein levels following CFA injection; 3) antisense oligodeoxynucleotides (ODN) specifically against NT-3 intrathecally administered during EA treatment for 7 days significantly attenuated the EA analgesia; and 4) the suppressed expression of spinal GFAP (astrocytic marker), OX-42 (microglial marker) as well as proinflammatory cytokines, interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha by EA treatment was significantly attenuated following NT-3 antisense ODN delivery. |
| 21680256 |
24498 |
Il6
|
Analgesia |
The present study demonstrated that: 1) repeated EA stimulation of ipsilateral GB30 and GB34 acupoints remarkably suppressed CFA-induced hyperalgesia; 2) EA treatment markedly enhanced the upregulation of spinal NT-3 mRNA and protein levels following CFA injection; 3) antisense oligodeoxynucleotides (ODN) specifically against NT-3 intrathecally administered during EA treatment for 7 days significantly attenuated the EA analgesia; and 4) the suppressed expression of spinal GFAP (astrocytic marker), OX-42 (microglial marker) as well as proinflammatory cytokines, interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha by EA treatment was significantly attenuated following NT-3 antisense ODN delivery. |
| 21695393 |
29335 |
Oprk1
|
Analgesia |
Intrarostral anterior cingulate cortex (rACC) administration of a kappa-, but not mu-opioid receptor antagonist, blocked EA action. These data demonstrate that EA activates opioid receptors in the rACC to inhibit the affective dimension of pain. |
| 21695393 |
25601 |
Oprm1
|
Analgesia |
Intrarostral anterior cingulate cortex (rACC) administration of a kappa-, but not mu-opioid receptor antagonist, blocked EA action. These data demonstrate that EA activates opioid receptors in the rACC to inhibit the affective dimension of pain. |
| 21799685 |
29595 |
Htr2a
|
Analgesia |
Serotonin Receptor 2A/C Is Involved in Electroacupuncture Inhibition of Pain in an Osteoarthritis Rat Model |
| 21799685 |
25187 |
Htr2c
|
Analgesia |
These data show that EA inhibits osteoarthritis-induced pain by enhancing spinal 5-HT2A/2C receptor activity |
| 21872220 |
25601 |
Oprm1
|
Analgesia |
Further, it has been demonstrated that spinal mu and delta, but not kappa opioid receptors are involved in EA-produced anti-hyperalgesia in complete Freund's adjuvant (CFA)-(Zhang et al., 2004) and capsaicin (Kim et al., 2009)-induced inflammatory and caudal trunk injury-induced neuropathic pain models |
| 21872220 |
24613 |
Oprd1
|
Analgesia |
Further, it has been demonstrated that spinal mu and delta, but not kappa opioid receptors are involved in EA-produced anti-hyperalgesia in complete Freund's adjuvant (CFA)-(Zhang et al., 2004) and capsaicin (Kim et al., 2009)-induced inflammatory and caudal trunk injury-induced neuropathic pain models |
| 21872220 |
29335 |
Oprk1
|
Analgesia |
Further, it has been demonstrated that spinal mu and delta, but not kappa opioid receptors are involved in EA-produced anti-hyperalgesia in complete Freund's adjuvant (CFA)-(Zhang et al., 2004) and capsaicin (Kim et al., 2009)-induced inflammatory and caudal trunk injury-induced neuropathic pain models |
| 22110373 |
24408 |
Grin1
|
Analgesia |
we studied p35 expression when electroacupuncture (EA) and a sub-effective dose of NMDA (N-methyl-D-aspartate) receptor antagonist (MK-801) were used to treat hyperalgesia in the diabetic neuropathic pain (DNP). |
| 22269805 |
81739 |
P2rx3
|
Analgesia |
Adenosine 5'-triphosphate disodium (ATP) gated P2X receptors, especially the subtype P2X3, play a key role in transmission of pain signals in neuropathic pain, ATP has been documented to play a significant role in the progression of pain signals, suggesting that control of these pathways through electroacupuncture (EA) is potentially an effective treatment for chronic neuropathic pain. |
