Protective effect of apigenin on cardiac function in rats with myocardial infarction and its possible mechanism
Miao Yanxia
Li Yan
Shi Baolin
Zhang Yueqi
Wu Chunli
Abstract：Objective To investigate the protective effect of apigenin on cardiac function in rats with myocardial infarction and its possible mechanism through deacetylase 3/β-catenin/peroxisome proliferator-activated receptor y(PPARγ)signaling pathway.Methods Forty healthy adult male specific pathogen-free SD rats were randomly divided into sham operation group,myocardial infarction group,apigenin group and apigenin+GW9662(a PPARγ antagonist)group,with 10 rats in each group.Myocardial infarction models were established in all groups except the sham operation group.Then the myocardial infarction group received no other intervention.The apigenin group was intraperitoneally injected with apigenin 5 mg/kg daily for 7 days,and the apigenin+GW9662 group was intraperitoneally injected with GW9662 2 mg/kg daily for 7 days on the basis of the apigenin group.The levels of myocardial enzymes,myocardial morphology,levels of inflammatory factors,apoptosis rate of myocardial cells,and the expression levels of deacetylase 3,β-catenin and PPARγ in myocardial tissue were compared among the groups.Results After the dead rats were removed,6 rats from each group were randomly selected for each test.The levels of creatine kinase isoenzymes and cardiac troponin Ⅰ in myocardial infarction group were significantly higher than those in sham operation group(both P＜0.001).However,the levels of both in apigenin group were significantly lower than those in myocardial infarction group[(41±6)U/L vs(118±14)U/L,(4.6±1.8)ng/L vs(14.2±2.2)ng/L](both P＜0.001).The levels of both in the apigenin+GW9662 group were significantly higher than those in the apigenin group(both P＜0.01).Compared with the myocardial infarction group,the apigenin group had better cell morphology and arrangement,clearer stripes,and less cell necrosis.The levels of interleukin-1β and interleukin-6 in apigenin group were significantly lower than those in myocardial infarction group(both P＜0.01),while the levels of interleukin-1 β and interleukin-6 in apigenin+GW9662 group were significantly higher than those in apigenin group(both P＜0.05).The apoptosis rates of myocardial cells in shamoperation group,myocardial infarction group,apigenin group,and apigenin+GW9662 group were 2.95％,38.78％,12.56％,and 22.33％,respectively.The levels of deacetylase 3 and PPARγ in apigenin group were significantly higher than those in myocardial infarction group,and the level of β-catenin was significantly lower in apigenin group than that in myocardial infarction group(all P＜0.001).The levels of deacetylase 3 and PPARγ in apigenin+GW9662 group were significantly lower than those in apigenin group(P＜0.05 or P＜0.01),and the level of β-catenin in apigenin+GW9662 group was significantly higher than that in apigenin group(P＜0.05).Conclusion Apigenin can significantly improve cardiac function and reduce cardiomyocyte apoptosis after myocardial infarction by activating deacetylase 3/β-catenin/PPARγ signaling pathway.The protective mechanism of apigenin may involve the regulation of this signaling pathway.Activation of PPARγ is essential for the cardioprotective effects of apigenin.
Keywords：Myocardial infarctionApigeninPeroxisome proliferation-activated receptors γSignaling pathway
Publication Date：2025-03-07
Online Publishing Date：2026-09-14(First online date of this platform, not the publication date of the document)
Pages：5( 346-350 )