| Evidence Sentence: |
Manual Acupuncture at ST37 Modulates TRPV1 in Rats with Acute Visceral Hyperalgesia via Phosphatidylinositol 3-Kinase/Akt Pathway |
| Evidence Sentence: |
Hyperalgesia is attenuated by inflammatory mediators that activate transient receptor potential vanilloid 1 (TRPV1), and TRPV1 is regulated by nerve growth factor (NGF)-induced phosphatidylinositol 3-kinase (PI3K)/Akt pathway. |
| Evidence Sentence: |
We demonstrated that MA at ST37 significantly decreased abdominal withdrawal reflex (AWR) scores, proinflammatory cytokine expression (TNF-alpha, IL-1beta, and IL-6), and TRPV1 protein and mRNA expression in rats with acute visceral hyperalgesia compared with the untreated controls, while MA at LI11 showed no effect. |
| Evidence Sentence: |
In rats with visceral hyperalgesia, the upregulation of NGF, tropomyosin-receptor-kinase A (TrkA), PI3K, and phosphorylation-Akt (p-Akt) was decreased by MA at ST37, indicating that TRPV1 regulation via the NGF-induced PI3K/Akt pathway plays a vital role in the effects of MA-mediated amelioration of acute visceral hyperalgesia. |
| Evidence Sentence: |
MA Treatment at ST37 Reduced TRPV1 mRNA Levels in the Colon via PI3K Pathway Induced by NGF |
| Evidence Sentence: |
NGF, TrkA, PI3K, and TRPV1 mRNA expressions in the colon of rats with acute visceral hyperalgesia were significantly higher than those in the normal control group. |
| Evidence Sentence: |
MA treatment at ST37, but not at LI11, could reduce NGF, TrkA, PI3K, Akt, and TRPV1 mRNA expression. |
| Evidence Sentence: |
Downregulation of PI3K, Akt, and TRPV1 mRNA expression due to MA treatment in the ST37 + IGF-1 group was blocked by IGF-1 treatment; significant differences in PI3K, Akt, and TRPV1 mRNA expression were observed between the ST37 + IGF-1 and ST37 (P < 0.05) groups. |
| Evidence Sentence: |
PI3K, Akt, and TRPV1 mRNA expressions were upregulated by the PI3K agonist IGF-1 in the IGF-1 group, compared to those in the model group (P < 0.05). |
| Evidence Sentence: |
MA Treatment at ST37 Reduced TRPV1 Protein Expression in the Colon via NGF-Mediated PI3K Pathway Modulation |
| Evidence Sentence: |
The expression of NGF, TrkA, PI3K, p-Akt, and TRPV1 proteins was significantly higher in the colons of rats with acute visceral hyperalgesia than in those of healthy controls (P < 0.05). |
| Evidence Sentence: |
MA treatment at ST37, but not LI11, could reduce NGF, TrkA, PI3K, p-Akt, and TRPV1 protein expression. |
| Evidence Sentence: |
The downregulation of PI3K and TRPV1 protein expressions after MA treatment in the ST37 + IGF-1 group was reversed by treatment with IGF-1. |
| Evidence Sentence: |
Significant differences in PI3K, p-Akt, and TRPV1 protein expression were observed between the ST37 + IGF-1 and ST37 groups (P < 0.05), and no differences were observed between the ST37 + IGF-1 and model groups (P > 0.05). |
| Evidence Sentence: |
PI3K, p-Akt, and TRPV1 protein expression in the IGF-1 group increased significantly after treatment with the PI3K agonist IGF-1, compared to that in the model group (P < 0.05). |
