Electroacupuncture alleviates water avoidance stress-induced irritable bowel syndrome in mice by improving intestinal barrier functions and suppressing the expression of inflammatory cytokines.

OBJECTIVE: To evaluate the effects and related mechanisms of electroacupuncture (EA) on irritable bowel syndrome (IBS). METHODS: Male C57BL/6 mice were randomly allocated into normal, model, and EA groups. Experimental IBS mice models were established by exposure to water avoidance stress (WAS). Mice in the EA group were treated with EA at bilateral Tianshu (ST 25) and Zusanli (ST 36) for 7 consecutive days, 15 min each day. Abdominal withdrawal reflex (AWR) tests and intestinal motility tests were performed to evaluate visceral sensitivity and intestinal motility of mice. Expression levels of tight junction proteins (TJPs) and inflammatory cytokines in colon tissues were determined through immunofluorescence, real-time polymerase chain reactions (PCR) and Western blot assays. RESULTS: EA alleviated visceral hypersensitivity and intestinal hypermotility in WAS-induced IBS mice. Moreover, EA promoted the expression of zonula occludens (ZO)-1, claudin-1, and occludin while suppressing the expression of interleukin (IL)-8, interferon (IFN)-γ, and tumor necrosis factor (TNF)-αin water avoidance stress (WAS)-induced irritable bowel syndrome (IBS) mice. CONCLUSION: EA alleviated WAS-induced IBS in mice by promoting intestinal barrier functions and suppressing the expression of inflammatory cytokines.

Electroacupuncture at Tianshu (ST25) and Zusanli (ST36) alleviates stress-induced irritable bowel syndrome in mice by modulating gut microbiota and corticotropin-releasing factor.

OBJECTIVE: To investigate whether electroacupuncture (EA) at bilateral Tianshu (ST25) and Zusanli (ST36) acupoints could alleviate stress-induced irritable bowel syndrome (IBS) and evaluate its effect on gut microbiota and corticotropin-releasing factor (CRF). METHODS: Thirty C57BL/6 mice were randomly divided into the normal, water avoidance stress (WAS), and WAS+EA groups (10 mice per group). An experimental model of IBS was established by exposing the animals to WAS. The mice were treated with EA at the bilateral Tianshu (ST25) and Zusanli (ST36) acupoints. The abdominal withdrawal reflex test was conducted to evaluate visceral sensitivity in IBS. Gut microbiota was analyzed using 16S rRNA sequencing and analysis. The expression of CRF was determined using immune-ofluorescence and quantitative real-time polymerase chain reaction. RESULTS: EA alleviated visceral hypersensitivity in a mouse model of WAS-induced IBS. It modulated the dysbiosis of gut microbiota induced by WAS. Moreover, it suppressed the WAS-induced overexpression of CRF in colon tissues. CONCLUSION: The findings of this study suggest that EA alleviated WAS-induced IBS mechanisms possibly involving the modulation of the dysbiosis of gut microbiota and suppression of CRF expression.