Lidocaine improves cardiac function in rats with myocardial ischemia-reperfusion by regulating mitochondrial autophagy
Objective To investigate the mechanism of lidocaine improving cardiac function by regulating mitochondrial autophagy in rats with myocardial ischemia-reperfusion injury.Methods Rats were randomly divided into sham operation group,model group,lidocaine group,autophagy inhibitor trimethyladenine(3-MA)group,and lidocaine+3-MA group,and the rat model of myocardial ischemia-reperfusion injury was established.The left ventricular function was detected by ultrasound,and the changes of left ventricular end-systolic diameter(LVESD),left ventricular end-diastolic diameter(LVEDD),left ventricular ejection fraction(LVEF),and left ventricular fractional shortening(FS)were observed.The myocardial infarct size was detected by TTC staining;the levels of CK-MB and cTnI in serum of rats in each group were detected by ELISA method.The pathological changes of myocardial tissues were observed by HE staining.The protein expressions of PINK1/Parkin,LC3 Ⅱ/Ⅰ,p62,and USP30 in myocardial tissues of rats in each group were detected by Western blot.Results Compared with the model group,the LVEF％and FS％of rats in the lidocaine group were significantly increased,LVEDD and LVESD were significantly decreased,the pathological changes of myocardial tissues were alleviated,the myocardial infarct size was significantly reduced,the levels of CK-MB and cTnI were significantly decreased,the protein expressions of PINK1,Parkin,LC3 Ⅱ/Ⅰ and USP30 were significantly increased,and the protein expression of p62 was significantly decreased.The above indexes were aggravated in the 3-MA group,and the effect of lidocaine on improving myocardial ischemia-reperfusion injury was weakened or inhibited by 3-MA.Conclusion Lidocaine improves cardiac function in rats with myocardial ischemia-reperfusion by regulating mitochondrial autophagy,and its mechanism may be related to the regulation of Pink1/Parkin signaling pathway.
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