In vivo and in vitro impact of atorvastatin against myocardial ischaemia-reperfusion injury by upregulation of silent information regulator l and attenuation of endoplasmic reticulum stress-induced apoptosis

被引:4
|
作者
Li, Fei [1 ]
Chang, ZiJuan [2 ]
Li, Ying [2 ]
Sun, Junjie [3 ]
机构
[1] YanTaiShan Hosp, Ward Cardiovasc Med 1, Yantai, Shandong, Peoples R China
[2] Qingdao Univ, Affiliated Yantai Yuhuangding Hosp, Dept Emergency, 20 Yuhuangding East Rd, Yantai 264000, Shandong, Peoples R China
[3] Qingdao Univ, Affiliated Yantai Yuhuangding Hosp, Dept Ultrason Med, 20 Yuhuangding East Rd, Yantai 264000, Shandong, Peoples R China
关键词
Atorvastatin; ER stress; apoptosis; SIRT1; HYPOXIA/REOXYGENATION INJURY; OXIDATIVE STRESS; CARDIOMYOCYTES; INHIBITION; MECHANISMS; PROTECTS;
D O I
10.1080/1061186X.2022.2091577
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
We aimed to investigate the effects and mechanism of Atorvastatin on Myocardial Ischaemia-Reperfusion Injury in vitro and in vivo. The effects of Atorvastatin on Silent information regulator l (SIRT1) and endoplasmic reticulum (ER) stress were investigated in Myocardial ischaemia-reperfusion (MI/R) injury rat model and hypoxia/reoxygenation (H/R)-treated H9c2 cells. Pathological changes, inflammatory and heart injury markers, cell apoptosis and cell death, SIRT1 and cleaved Caspase-12 expressions, and ER stress relative proteins were measured through HE, enzyme-linked immunosorbent assay, quantitative TUNEL and flow cytometry, immunofluorescence and Western blotting with the assistance of the SIRT1 specific inhibitor EX527 and ER stress pathway blocker treatment. The results of our study demonstrated that atorvastatin treatment attenuated MI/R and H/R mediated inflammatory and heart injury markers, cell apoptosis and cell death, SIRT1 and cleaved Caspase-12 expressions, and ER stress relative protein levels. Finally, we found that atorvastatin reversed SIRT1 expression and blockade the ER stress pathway and increase the cardiomyocytes survival rate in the presence of MI/R and H/R. Our findings provided a new rationale for subsequent academic and clinical research on MI/R injury.
引用
收藏
页码:1076 / 1087
页数:12
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