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白藜芦醇通过AT1R-ERK/p38丝裂原活化蛋白激酶信号通路改善糖尿病诱导的心脏功能障碍。

Resveratrol Ameliorates Diabetes-Induced Cardiac Dysfunction Through AT1R-ERK/p38 MAPK Signaling Pathway.

作者信息

Gao Yonglin, Kang Le, Li Chunmei, Wang Xiaoyan, Sun Chengfeng, Li Qingzhong, Liu Ruihua, Wang Jianping

机构信息

School of Life Sciences, Yantai University, Yantai, 264005, Shandong, People's Republic of China.

School of Pharmacy, Yantai University, Yantai, 264005, Shandong, People's Republic of China.

出版信息

Cardiovasc Toxicol. 2016 Apr;16(2):130-7. doi: 10.1007/s12012-015-9321-3.

DOI:10.1007/s12012-015-9321-3
PMID:25800751
Abstract

The present study was to determine the preventive effect of resveratrol (Res) on diabetes-induced cardiac dysfunction and the possible signaling pathway involved. Diabetes was induced in rats by injection of streptozotocin (STZ) at 45 mg/kg. The animals were randomly divided into three groups (10 rats/group): normal group, diabetes groups with or without Res (80 mg/kg) treatment. Biochemistry, cardiac function and fibrosis were detected. Moreover, pro-inflammatory cytokines were evaluated, and heart tissues were homogenized for western blot analysis to analyze the possible mechanisms. The results indicated that Res might regulate glucose and lipid metabolism, ameliorate cardiac function and fibrosis response in STZ-induced diabetic rats. The protective effects were consistent with the inhibition of inflammatory factors such as TNF-α, IL-6 and IL-1β. In addition, Res favorably shifted STZ-induced AT1R, ERK1/2 and p38 MAPK activation in rat heart. In conclusion, the results suggested that Res attenuated diabetes-induced cardiac dysfunction, and the effects were associated with attenuation inflammatory response and down-regulation of AT1R-ERK/p38 MAPK signaling pathway.

摘要

本研究旨在确定白藜芦醇(Res)对糖尿病诱导的心脏功能障碍的预防作用以及可能涉及的信号通路。通过腹腔注射链脲佐菌素(STZ,45mg/kg)诱导大鼠糖尿病模型。将动物随机分为三组(每组10只大鼠):正常组、糖尿病组以及糖尿病Res(80mg/kg)治疗组。检测生化指标、心脏功能和纤维化情况。此外,评估促炎细胞因子,并将心脏组织匀浆进行蛋白质印迹分析以分析可能的机制。结果表明,Res可能调节STZ诱导的糖尿病大鼠的糖脂代谢,改善心脏功能和纤维化反应。其保护作用与抑制TNF-α、IL-6和IL-1β等炎症因子一致。此外,Res可改善STZ诱导的大鼠心脏中AT1R、ERK1/2和p38 MAPK的激活。总之,结果表明Res减轻了糖尿病诱导的心脏功能障碍,其作用与减轻炎症反应和下调AT1R-ERK/p38 MAPK信号通路有关。

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