| 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: |
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 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 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: |
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). |
