Downregulation of microRNA‐155 stimulates sevoflurane‐mediated cardioprotection against myocardial ischemia/reperfusion injury by binding to SIRT1 in mice

Abstract

Objective The inhaled sevoflurane has been demonstrated to protect against myocardial ischemia/reperfusion (I/R) injury. However, the relative mechanisms of sevoflurane‐mediated cardioprotection remain largely unknown. This study intends to explore the effect of miR‐155 on the sevoflurane‐mediated cardioprotection by regulating Sirtuin 1 (SIRT1) in mouse models of myocardial I/R. Methods Left anterior descending coronary artery ligation was used to induce models of myocardial I/R in mice. The I/R mice were treated with sevoflurane, sevoflurane + mimics negative control (NC) or sevoflurane + miR‐155 mimics. The expression of microRNA‐155 (miR‐155) and SIRT1 was examined by quantitative real‐time polymerase chain reaction and Western blot assay. Then cardiac functions and hemodynamic alterations were evaluated. Evans blue‐2,3,5‐triphenyltetrazolium chloride and terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling assay staining methods were adopted to evaluate infarct size and cardiomyocyte apoptosis, respectively. Results In the I/R mice, miR‐155 was expressed at a high level and SIRT1 at a low level. SIRT1 was confirmed to be a target gene of miR‐155. The treatment of sevoflurane could reduce miR‐155 expression and increased SIRT1 expression in the myocardial tissues, under which conditions, cardiac functions were promoted, accompanied by reduced infarct size and inhibited cardiomyocyte apoptosis. In response to miR‐155 upregulation, the sevoflurane‐treated I/R mice showed reduced cardiac functions, and increased infarct size and cardiomyocyte apoptosis. Conclusion The findings obtained in this study provide evidence suggesting that miR‐155 targets and negatively regulates SIRT1 expression, a mechanism by which the protection of sevoflurane is inhibited against myocardial I/R in mice.

MicroRNA‑494 suppresses hypoxia/reoxygenation‑induced cardiomyocyte apoptosis and autophagy via the PI3K/AKT/mTOR signaling pathway by targeting SIRT1

“…as an essential member of the seven categories of the sirtuin protein family, SirT1 is considered as a critical regulator of cell apoptosis and autophagy (45). recently, numerous studies reported that SirT1 was involved in myocardial i/r injury (46,47). ding et al (48) demonstrated that mir-29a inhibition could activate SirT1, thus preventing i/r injury by inhibiting oxidative stress.…”

MicroRNA‐203–mediated inhibition of doublecortin underpins cardioprotection conferred by sevoflurane in rats after myocardial ischaemia‐reperfusion injury

“…16 Increasing evidence supports a protective role of SEV in myocardial I/R injury. 17,18 The current study was designed to investigate specific molecular mechanisms with the previous finding that SEV is protective against myocardial I/R injury. 4 Also, SEV post-conditioning treatment has been noted to alleviate hypoxia-reoxygenation injury in cardiomyocytes.…”

miR‑155‑5p downregulation inhibits epithelial‑to‑mesenchymal transition by targeting SIRT1 in human nasal epithelial cells

“…A previous study reported that SIRT1 attenuates nasal polypogenesis through EMT suppression ( 48 ). Furthermore, it has been demonstrated that SIRT1 is a target gene of miR-155-5p ( 49 ). Huang et al ( 49 ) reported that miR-155 downregulation stimulated cardioprotection against myocardial ischemia/reperfusion injury by binding to SIRT1.…”

“…Furthermore, it has been demonstrated that SIRT1 is a target gene of miR-155-5p ( 49 ). Huang et al ( 49 ) reported that miR-155 downregulation stimulated cardioprotection against myocardial ischemia/reperfusion injury by binding to SIRT1. However, the role of miR-155-5p in inhibiting EMT has not been extensively reported.…”