Role of microRNA‐145 in protection against myocardial ischemia/reperfusion injury in mice by regulating expression of GZMK with the treatment of sevoflurane. Issue 9 (14th March 2019)

• Record Type: Journal Article
• Authors: Qi, Zheng; Li, Shushan; Su, Yu; Zhang, Ji; Kang, Yu; Huang, Yunli; Jin, Feng; Xing, Qinghe
• Is Part Of: Journal of cellular physiology. Volume 234:Issue 9(2019:Sep.)
• Page Start: 16526
• Page End: 16539
• Publication Date: 2019-03-14
• Subjects: cardiomyocyte apoptosis -- GZMK -- microRNA‐145 -- myocardial ischemia/reperfusion injury -- sevoflurane; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.28323
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: This study aims to investigate the role of microRNA‐145 (miR‐145) in protection against myocardial ischemia/reperfusion (I/R) injury in mice by regulating expression of granzyme K (GZMK) with the treatment of sevoflurane. The mice model of myocardial I/R injury was established by left coronary artery ligation. The expression of miR‐145 and GZMK in myocardial tissues of mice was detected by Reverse transcription quantitative polymerase chain reaction and western blot analysis. The changes of the cardiac function and hemodynamics, pathological changes of myocardial tissues, the ultrastructure of cardiomyocytes, myocardial infarction area, and cardiomyocyte apoptosis were observed. The expression of the apoptosis‐related protein cleaved‐caspase‐3, Bax, and Bcl‐2 was detected by western blot analysis. The levels of malondialdehyde, myeloperoxidase, superoxide dismutase in myocardial tissues were detected by spectrophotometric colorimetry. The levels of interleukin‐1β (IL‐1β), IL‐6, and tumor necrosis factor‐α in the serum of mice were detected by the enzyme‐linked immunosorbent assay. The level of oxidative stress and the expression of inflammatory factors increased in mice with myocardial I/R injury. Sevoflurane postconditioning could reduce myocardial I/R injury in mice. Sevoflurane postconditioning may protect myocardial I/R injury through miR‐145‐regulation of GZMK in mice. Inhibition of miR‐145 expression could reduce the protective effect of sevoflurane posttreatment on myocardial I/R injury in mice. Low expression of GZMK could attenuate the inhibitory effect of miR‐145 on myocardial I/R injury after sevoflurane treatment in mice. Our study suggests that sevoflurane postconditioning may protect against myocardial I/R injury by upregulating miR‐145 expression and downregulating GZMK expression.