Myocardial Protective Effect of Gambogic Acid on Rats with Myocardial Ischemia/Reperfusion Injury by Regulating PI3K/AKT Signaling Pathway
Objective:To investigate the impacts of gambogic acid(GA) on the phosphatidylinositol-3-kinase/protein kinase B(PI3K/AKT) signaling pathway and myocardial injury in myocardial ischemia-reperfusion injury (MIRI) rats.Methods:Rats were randomly grouped into sham surgery group(Sham group),model group(Model group),GA group,and GA+PI3K inhibitor LY294002 group(GLY group).The rats in Sham group only threaded without ligation,while the rats in other groups constructed MIRI models,the pathological changes of myocardial tissue were observed,and the apoptosis rate of myocardial cells,myocardial injury markers[cardiac troponin I(cTnI),lactate dehydrogenase(LDH),creatine kinase-MB(CK-MB)],inflammatory factors[interleukin(IL)-1β,IL-18,IL-6,tumor necrosis factor-α(TNF-α)],and the expression of Bax,Bcl-2,cleaved-capase 3,p-PI3K,PI3K,p-AKT,and AKT proteins in myocardial tissue of MIRI rats were detected.Results:The GA group showed loose arrangement of myocardial fibers,infiltration of a small amount of inflammatory cells,and mild myocardial injury.Compared with Model group,the apoptosis rate,Bax,cleaved-capase 3,cTnI,LDH,CK-MB,IL-1β,IL-18,IL-6,and TNF-αin GA group reduced obviously(P<0.05),the expression of Bcl-2,p-PI3K/PI3K,and p-AKT/AKT proteins increased obviously(P<0.05). Compared with GA group,the apoptosis rate,Bax,cleaved-capase 3,cTnI,LDH,CK-MB,IL-1β,IL-18,IL-6,and TNF-αin GLY group increased obviously(P<0.05),the expression of Bcl-2,p-PI3K/PI3K,and p-AKT/AKT proteins reduced obviously(P<0.05).Conclusion:GA inhibits inflammatory response,inhibits cardiomyocyte apoptosis,reduces MIRI in rats,and exerts myocardial protective effects by activating the PI3K/AKT signaling pathway.
myocardial ischemia/reperfusion injurymyocardial protectiongambogic acidphosphatidylinositol 3-kinase/protein kinase Bexperimental study
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