Objective To investigate the protective effect of capsaicin on acute myocardial infarction rats and its related mechanism.Methods Network pharmacologyanalysis was conducted in conjunction with TCMSP,DAVID and other websites to explore the possible action targets and pathways of capsaicin.Forty-eight SD rats were randomly divided into sham operation group,model group,capsaicin(20 mg/kg)group,and capsaicin+2-MeoE2(30 mg/kg)group.Each group was given the corresponding drug intragastrically for 14 days,once daily.The changes of myocardial function in rats with acute myocardial infarction were observed by echocardiography.Serum levels of CK,CK-MB,LDH,and cTnT were detected by the kit.HE staining was used to observe the histological changes of the heart tissue.Real-time fluorescence quantitative detection of HIF-1A,VEGF,HMOX1,Bcl-2 mRNA expression.The protein levels of HIF-1A and Bcl-2 in rat myocardia were detected by Western blotting.Results Network pharmacology analysis showed that the HIF-1 signaling pathway was the most significant pathway for capsaicin to inhibit the accumulation of targets in acute myocardial infarction.Animal experiments showed that compared with model group,the apoptosis rate of cardiomyocytes in capsaicin group was significantly reduced,serum CK,CK-MB,LDH and cTnT levels were significantly decreased,and left ventricular end-diastolic volume(LVEDV)and left ventricular end-systolic volume(LVESV)were significantly decreased.The left ventricular short axis shortening rate(LVFS),left ventricular ejection fraction(LVEF)and stroke volume(SV)were significantly increased(P<0.05,0.01),while the mRNA expressions of HIF-1A,VEGF,HMOX1 and Bcl-2 were significantly increased.The expressions of HIF-1A and Bcl-2 were also significantly increased(P<0.01).Compared with capsaicin group,the protective effect of capsaicin+2-MeoE2 group on acute myocardial infarction rats was significantly weakened.Conclusion Capsaicin may interfere with the activity of HIF-1 and other signaling pathways by regulating HIF-1A,VEGF,HMOX1,Bcl-2 and other core targets,and thus play an anti-acute myocardial infarction role.
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