Beta-arrestin2 is involved in the increase of distal colonic contraction in diabetic rats

Regulatory Peptides Pub Date : 2013-08-10 DOI:10.1016/j.regpep.2013.06.006

Dong-Ping Xie , Sen Li , Liang Li , Xin-Wen Chang , Tao-Fang Xi , Xiao Yang , Zhi Jin , Ying Zeng

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引用次数: 6

Abstract

Colonic dysmotility occurs in diabetes and the patients exhibit diarrhea or constipation. The pathogenetic mechanisms underlying colonic dysmotility in diabetic patients remain poorly understood. The effects of β-arrestin2 on colonic contraction in diabetic rats were investigated for the first time. Male SD rats were treated with a single intraperitoneally injected dose of streptozotocin, and those displaying sustained high blood glucose were selected as diabetes mellitus models. Longitudinal muscle strips of the distal colon were prepared to monitor contraction of the colon in vitro. Expression of β-arrestin2 was investigated by Western blot analysis. Anti-β-arrestin2 antibody had no direct effect on the contraction of distal colonic strips in both normal and diabetic rats. Carbachol-induced contractions of distal colonic strips were higher in diabetic rats than in normal rats. Anti-β-arrestin2 antibody partly blocked carbachol-induced increases of distal colonic strips in diabetic rats. The expression level of β-arrestin2 protein in the colon was higher in diabetic rats than in normal rats. These results suggest that β-arrestin2 is involved in the increase of distal colonic contraction in diabetic rats.

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β -arrestin2参与糖尿病大鼠远端结肠收缩的增加

糖尿病患者出现结肠运动障碍，患者表现为腹泻或便秘。糖尿病患者结肠运动障碍的发病机制尚不清楚。本文首次观察β-阻滞2对糖尿病大鼠结肠收缩的影响。雄性SD大鼠单次腹腔注射链脲佐菌素，将持续高血糖的大鼠作为糖尿病模型。制备远端结肠纵肌条，在体外监测结肠收缩。Western blot检测β-arrestin2的表达。抗β-arrestin2抗体对正常大鼠和糖尿病大鼠远端结肠条带的收缩无直接影响。糖尿病大鼠的远端结肠条收缩率明显高于正常大鼠。抗β-arrestin2抗体部分阻断了碳巴酚诱导的糖尿病大鼠远端结肠条带的增加。糖尿病大鼠结肠中β-arrestin2蛋白的表达水平高于正常大鼠。提示β-arrestin2参与糖尿病大鼠远端结肠收缩的增加。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Regulatory Peptides 医学-内分泌学与代谢

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审稿时长

2 months

期刊介绍： Regulatory Peptides provides a medium for the rapid publication of interdisciplinary studies on the physiology and pathology of peptides of the gut, endocrine and nervous systems which regulate cell or tissue function. Articles emphasizing these objectives may be based on either fundamental or clinical observations obtained through the disciplines of morphology, cytochemistry, biochemistry, physiology, pathology, pharmacology or psychology.