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

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• 作者：Yonglin Gao ; Le Kang ; Chunmei Li ; Xiaoyan Wang ; Chengfeng Sun…
• 关键词：Resveratrol ; Diabetes ; induced cardiac dysfunction ; Glucose and lipid metabolism ; Inflammation response ; AT1R ; ERK/p38 MAPK
• 刊名：Cardiovascular Toxicology
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：16
• 期：2
• 页码：130-137
• 全文大小：904 KB
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• 作者单位：Yonglin Gao (1)
  Le Kang (1)
  Chunmei Li (2)
  Xiaoyan Wang (1)
  Chengfeng Sun (1)
  Qingzhong Li (1)
  Ruihua Liu (3)
  Jianping Wang (3)
  
  1. School of Life Sciences, Yantai University, Yantai, 264005, Shandong, People’s Republic of China
  2. School of Pharmacy, Yantai University, Yantai, 264005, Shandong, People’s Republic of China
  3. Yantai Yuhuangding Hospital, Yantai, 264000, Shandong, People’s Republic of China
  
• 刊物主题：Pharmacology/Toxicology; Cardiology;
• 出版者：Springer US
• ISSN：1559-0259

文摘

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.