电针通过改善肠道屏障功能和抑制炎性细胞因子的表达,减轻小鼠避水应激性肠易激综合征。

Sun Mengzhu, Zhang Yujie, Song Yafang, Guo Jing, Wang Yuhang, Xin Chen, G U Dongmei, Sun Jianhua, Pei Lixia
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引用次数: 0

摘要

目的:探讨电针治疗肠易激综合征(IBS)的疗效及相关机制。方法:雄性C57BL/6小鼠随机分为正常组、模型组和EA组。采用避水应激法(WAS)建立IBS小鼠模型。EA组小鼠在双侧天枢穴(ST 25)和足三里穴(ST 36)连续治疗7天,每天15分钟。采用腹部戒断反射(AWR)试验和肠蠕动试验评价小鼠内脏敏感性和肠蠕动。通过免疫荧光、实时聚合酶链反应(PCR)和Western blot检测结肠组织中紧密连接蛋白(TJPs)和炎性细胞因子的表达水平。结果:EA减轻了was诱导的IBS小鼠内脏超敏反应和肠道运动亢进。此外,EA促进了水回避应激(WAS)诱导的肠易激综合征(IBS)小鼠中闭塞带(ZO)-1、cludin -1和occludin的表达,同时抑制了白细胞介素(IL)-8、干扰素(IFN)-γ和肿瘤坏死因子(TNF)-α的表达。结论:EA可通过促进肠道屏障功能和抑制炎症因子表达来减轻was诱导的小鼠IBS。
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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.

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