阿托伐他汀
内质网
未折叠蛋白反应
细胞凋亡
标记法
再灌注损伤
下调和上调
半胱氨酸蛋白酶12
体内
医学
程序性细胞死亡
药理学
缺血
流式细胞术
细胞生物学
半胱氨酸蛋白酶
化学
免疫学
生物
内科学
生物化学
生物技术
基因
作者
Fĕi Li,Zhiqiang Chang,Ying Li,Jin Sun
标识
DOI:10.1080/1061186x.2022.2091577
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.
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