Evidence Details for Igf1
PMID Title Journal Year Abstract
34646326 Manual Acupuncture at ST37 Modulates TRPV1 in Rats with Acute Visceral Hyperalgesia via Phosphatidylinositol 3-Kinase/Akt Pathway. Evid Based Complement Alternat Med. 2021 Oct 4;2021:5561999. doi: 10.1155/2021/5561999. eCollection 2021. 2021 Acupuncture can significantly ameliorate inflammatory pain in acute visceral hyperalgesia. 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. However, it is unknown whether NGF-induced PI3K/Akt pathway is associated with manual acupuncture (MA). In this study, the effect and mechanism of MA at Shangjuxu (ST37) and Quchi (LI11) were examined using an acetic acid-induced rat model with visceral hyperalgesia. 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. The effects of MA at ST37 were reversed after treatment with the PI3K agonist IGF-1 30 min before MA. 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: The effects of MA at ST37 were reversed after treatment with the PI3K agonist IGF-1 30 min before MA.
Evidence Sentence: Moreover, the effects of MA at ST37 were inhibited by the administration of the PI3K agonist IGF-1; the ST37 + IGF-1 group showed significant differences when compared to the ST37 group (P < 0.05), but not the IGF-1 group (P > 0.05; Figure 2).
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: Downregulation of NGF and TrkA mRNA expression by MA treatment at ST37 was still observed, with significant differences between the ST37 + IGF-1 and model groups (P < 0.05).
Evidence Sentence: NGF and TrkA mRNA expressions in the ST37 + IGF-1 group were not affected by IGF-1 treatment, while there are no differences in NGF and TrkA mRNA expressions between the IGF-1 and model groups (P > 0.05; Figure 4).
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).
Evidence Sentence: However, downregulation of NGF and TrkA protein expressions due to MA treatment at ST37 was still observed, with significant differences between the ST37 + IGF-1 and model groups (P < 0.05).
Evidence Sentence: NGF and TrkA protein expressions were not affected by IGF-1 treatment, and there were no significant differences in NGF and TrkA expressions between the IGF-1 and model groups (P > 0.05) (Figure 5).