[Involvement of Pirt /TRPV1 signaling in acupuncture-induced reduction of visceral hypersensitivity in diarrhea-predominant irritable bowel syndrome rats].

医学 肠易激综合征 足三里 TRPV1型 电针 腹泻 胃肠病学 内科学 针灸科 排便 腹痛 刺激 退缩反射 结肠炎 艾灸 麻醉 瞬时受体电位通道 受体 病理 替代医学
作者
Ying Chen,Yan Zhao,Lu Wang,Junpeng Yao,Ying Li,Siyuan Zhou
出处
期刊:Acupuncture Research 卷期号:46 (4): 278-283 被引量:4
标识
DOI:10.13702/j.1000-0607.200442
摘要

Objective To observe the effect of electroacupuncture (EA) on the expression of Pirt (a regulator of TRPV1) in the dorsal root ganglia (DRG) and transient receptor potential vanilloid 1 (TRPV1, a molecular sensor of noxious heat and capsaicin) in the colonic mucosa in rats suffering from diarrhea-predominant irritable bowel syndrome (IBS-D), so as to explore its mechanisms underlying alleviation of visceral hypersensitivity of IBS-D. Methods Forty SD rats (half male and half female) were randomly assigned to control, model, EA, and medication groups by lottery, with 10 rats in each group. The IBS-D model was established by chronic unpredictable mild stress (CUMS) and gavage of senna soaking fluid. Rats in the EA group received EA (2 Hz/15 Hz,0.1-1 mA) stimulation of unilateral Tianshu(ST25), Zusanli (ST36), Sanyinjiao(SP6) and Taichong(LR3) for 15 min once a day for 14 days, and rats of the medication group received intragastric administration of pinave-rium bromide (10 mL/kg, 2.7 mg/mL) once daily for 14 days. The visceral pain threshold (VPT) was measured by using abdominal wall withdrawal reflex (AWR) test. The diarrhea index (loose stool rate [total number of loose stool/total number of defecation] X mean loose degree [0-4 grades according to the filter paper stain diameter] in 6 h/d) was used to assess the severity of diarrhea. The expression of Pirt in the DRG and TRPV1 in the colonic mucosa tissue was detected using immunohistochemistry. Results After modeling, the VPT was obviously reduced (P 0.05). Conclusion EA can effectively alleviate visceral hypersensitivity in IBS-D rats, which may be related to its effect in down-regulating the expression level of DRG Pirt and colonic TRPV1.
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