Resveratrol ameliorates diabetic myocardial injury through HSF1-mediated ferroptosis

• 作者: Zhen-Wang Ma De-You Jiang Bing-Cheng Hu Xing-Xing Yuan Mei Wang Hai-Long Li Shao-Jie Cai Jing Guo
• 来源期刊: 海南医科大学学报（英文版）
• 年，卷（期）: 2022,（6）
• 所属期刊栏目: Original article
• 页码范围: 6-11
• 页数: 6页
• 语种: 英文

摘要

Objective: To observe the effect of resveratrol on the injury of diabetic cardiomyocytes and its effect on HSF1 mediated iron death. Methods: the diabetic cardiomyopathy model was established by high glucose induced H9c2, and H9c2 was exposed to normal glucose concentration as a control. Then the intervention was performed with the corresponding drugs. The cell proliferation level was detected by CCK8 method, the concentrations of LDH, SOD, MDA and iron ions were detected by kit method, and the expression levels of HSF1, apoptotic proteins (Bax and Bcl-2) and iron death marker proteins (ACSL4, GPX4 and SLC7A11) were detected by Western blot; Results: compared with the blank group, the cell activity, SOD activity, the expression of HSF1, Bcl-2, GPX4 and SLC7A11 protein in the model group decreased significantly, and the LDH activity, MDA content, Bax and ACSL4 protein expression, Bax/Bcl-2 ratio and Fe2+ content increased significantly (P<0.01). Compared with the model group, the activity of H9c2 cells, the activity of SOD, the expression of HSF1, Bcl-2, GPX4 and SLC7A11 protein increased significantly, and the activity of LDH, the content of MDA, the expression of Bax and ACSL4 protein, the ratio of Bax/Bcl-2 and the content of Fe2+ decreased significantly in the resveratrol group (P<0.01). After the intervention, the activity of H9c2 cells, the activity of SOD, the expression of HSF1, Bcl-2, GPX4 and SLC7A11 protein decreased significantly, and the activity of LDH, the content of MDA, the expression of Bax and ACSL4 protein, the ratio of Bax/Bcl-2 and the content of Fe2+ increased significantly in si-hsf1 group (P<0.01); Conclusion: resveratrol can inhibit cell iron death and improve high glucose induced cardiomyocyte injury by up regulating the expression of HSF1.