[Mechanism of electroacupuncture against intestinal inflammation in mice with Parkinson's di-sease by NF-κB/IL-6 pathway].

OBJECTIVE

To observe the effects of electroacupuncture (EA) at "Fengfu"(GV16), "Taichong"(LR3), and "Zusanli"(ST36) on the tyrosine hydroxylase (TH), nuclear factor-kappa B (NF-κB), interleukin (IL)-6, and zonula occludens-1 (ZO-1) in mice with Parkinson's disease (PD), and to explore the underlying mechanism of EA in the treatment of PD.

METHODS

C57BL/6 mice were randomly divided into control, model, and EA groups, with 10 mice in each group. The PD model was induced by rotenone (i.g.) in mice for 28 d. EA was applied to GV16, LR3 and ST36 of mice in the EA group for 30 min, once daily for 14 d. The behavioral changes of mice in each group before and after treatment were observed and scored. The total distance traveled autonomously of mice was detected in the open field test. TH expression in the substantia nigra (SN) was measured by immunohistochemistry, and the changes in colon tissue structure were observed by HE staining. The intestinal mRNA expression of ZO-1, NF-κB, and IL-6 was detected by quantitative real-time PCR, and the colon tissue protein expression of NF-κB was detected by Western blot. The colon tissue concentration of IL-6 was detected by ELISA.

RESULTS

Compared with the control group, the pre- and post-treatment behavioral scores of the model group and the pre-treatment behavioral score of the EA group were increased (<0.01). Compared with the model group, the EA group showed reduced behavioral score after treatment (<0.01). Compared with the control group, the model group showed reduced goblet cells and crypts and thinner muscle layer in the intestinal specimens of mice. Compared with the model group, the EA group showed intact surface villi, increased goblet cells and crypts, and thickened muscle layer. Compared with the control group, the model group exhibited reduced total distance traveled in the open field test, TH expression in SN, and ZO-1 mRNA expression (<0.01), and elevated mRNA and protein expression of NF-κB and IL-6, and the ratio of p-NF-κB/NF-κB in the intestinal tract (<0.01). Compared with the model group, the EA group displayed increased total distance traveled, TH expression in SN, and ZO-1 mRNA expression (<0.01), and declining mRNA and protein expression of NF-κB and IL-6, and the ratio of p-NF-κB/NF-κB in the colon tissue (<0.01, <0.05).

CONCLUSION

EA at GV16, LR3, and ST36 can regulate the expression of NF-κB/IL-6, inhibit the transmission of the colon tissue inflammatory response, repair the intestinal barrier function, and potentiate the TH activity, thereby improving the behavioral performance of PD mice.