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链脲佐菌素诱导的糖尿病大鼠海马中磷酸化Smad2和Smad3表达增加。

Increased expression of phosphorylated Smad2 and Smad3 in the hippocampus of streptozotocin-induced diabetic rats.

作者信息

Bao Y, Jiang L, Shi Y-Q, Zou J-J, Zhao Y, Liu Z-M

机构信息

Department of Endocrinology, Changzheng Hospital, Second Military Medical University, Shanghai, China.

出版信息

Exp Clin Endocrinol Diabetes. 2010 Jan;118(1):47-50. doi: 10.1055/s-0029-1225610. Epub 2009 Oct 15.

DOI:10.1055/s-0029-1225610
PMID:19834880
Abstract

Activation of the Smad signalling pathway has been implicated in the pathological process of diabetic associated complications. The current study was designed to see whether Smad signalling was activated in the hippocampus of streptozotocin-induced diabetic rats. Compared with vehicle-treated controls, immunoblot analysis of hippocampal extracts showed that phosphorylated Smad2 was upregulated at 8 weeks post streptozotocin induction (p<0.01), and phosphorylated Smad3 protein was upregulated at 4 and 8 weeks post streptozotocin induction (p<0.01) in streptozotocin-induced diabetic rats. In addition, immunofluorescence labelling assay showed that the percentage of pSmad2 immunoreactive astrocytes increased significantly in CA1, CA3 and dentate gyrus region (p<0.01), and pSmad3 immunoreactive astrocytes increased significantly in CA1 region (p<0.01) and in CA3 and dentate gyrus region (p<0.05) of the hippocampus in diabetic rats. These data indicate that Smad signalling is enhanced in hippocampal astrocytes of diabetic rats, and may thereby represent a clue to explore its exact role in the development of diabetic encephalopathy.

摘要

Smad信号通路的激活与糖尿病相关并发症的病理过程有关。本研究旨在观察链脲佐菌素诱导的糖尿病大鼠海马中Smad信号是否被激活。与溶剂处理的对照组相比,对海马提取物进行免疫印迹分析显示,链脲佐菌素诱导的糖尿病大鼠在链脲佐菌素诱导后8周时磷酸化Smad2上调(p<0.01),在链脲佐菌素诱导后4周和8周时磷酸化Smad3蛋白上调(p<0.01)。此外,免疫荧光标记分析显示,糖尿病大鼠海马CA1、CA3和齿状回区域中pSmad2免疫反应性星形胶质细胞的百分比显著增加(p<0.01),海马CA1区域(p<0.01)以及CA3和齿状回区域(p<0.05)中pSmad3免疫反应性星形胶质细胞显著增加。这些数据表明,糖尿病大鼠海马星形胶质细胞中的Smad信号增强,这可能为探索其在糖尿病性脑病发展中的确切作用提供线索。

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