Upregulation of SIRT1 contributes to the cardioprotective effect of Rutin against myocardial ischemia-reperfusion injury in rats

被引:27
作者
Lin, Qiao [1 ,2 ,3 ]
Chen, Xiu-Ying [1 ,2 ,3 ]
Zhang, Ji [4 ]
Yuan, Yong-Liang [4 ]
Zhao, Wen [1 ,2 ,3 ]
Wei, Bo [1 ,2 ,3 ]
机构
[1] Zhengzhou Univ, Minist Educ China, Key Lab Adv Drug Preparat Technol, Zhengzhou 450001, Henan, Peoples R China
[2] Zhengzhou Univ, Coinnovat Ctr Henan Prov New Drug R&D & Preclin S, Zhengzhou 450001, Henan, Peoples R China
[3] Zhengzhou Univ, Sch Pharmaceut Sci, Zhengzhou 450001, Henan, Peoples R China
[4] Zhengzhou Univ, Affiliated Hosp 1, Dept Pharm, Henan Key Lab Precis Clin Pharm, Zhengzhou 450052, Henan, Peoples R China
基金
中国国家自然科学基金; 中国博士后科学基金;
关键词
Rutin; SIRT1; Nrf2; Oxidative stress; Myocardial ischemia reperfusion; TANSHINONE IIA SULFONATE; OXIDATIVE STRESS; ISCHEMIA/REPERFUSION INJURY; PROTECTS; PATHWAY; ACTIVATION; CARDIOMYOPATHY; INFARCTION; DYSFUNCTION; INHIBITION;
D O I
10.1016/j.jff.2018.05.007
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
The mechanisms underlying beneficial actions of Rutin, a food derived-polyphenolic bioflavonoid, against myocardial ischemia-reperfusion (MI/R) injury were detected. We found that Rutin could significantly ameliorate infarct size and attenuate cardiac dysfunctionto in some extent. Additionally, Rutin could also improve variation of myocardial zymogram and up-regulate antioxidant systems in heart. The selective SIRT1 inhibitor, Ex-527, exacerbated MI/R injury as evidenced by further increased oxidative stress and infracted area in heart tissue. Importantly, Ex-527 abolished the cardioprotective effect of Rutin in MI/R rats. Docking analysis further demonstrated the vital role of SIRT1 on Rutin's cardioprotective effect. We found that activation of SIRT1/Nrf2 signaling induced by Rutin contributes to the reduced oxidative stress, along with decreased apoptosis of cardiomyocytes in heart tissue. Overall, our findings suggest that SIRT1/Nrf2 signaling pathway may be a potential therapeutic target for the treatment of oxidative stress and apoptosis related myocardial diseases.
引用
收藏
页码:227 / 236
页数:10
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