Protective Effect Of Atractylodes ? And ? On The Heart After Myocardial Infarction In A Mice Model

Objectives:A substantial proportion of patients with acute myocardial infarction?AMI?do not receive reperfusion therapy.It is important to limit myocardial damage and improve the prognosis after MI,and the administration of antiplatelet drugs upstream of percutaneous coronary intervention has been shown to be beneficial for patients with AMI.The aim of this study is that if patients with AMI who do not receive reperfusion therapy could benefit from pretreatment with atractylodes lactone ???.Methods:Study mice were randomly divided into eight groups:?1?sham group;?2?control group;?3?atractylodes lactone ??? low dose group[atractylodes lactone ????5 mg/kg?intragastricly administered before MI];?4?atractylodes lactone ??? middle dose group[atractylodes lactone ????30 mg/kg?intragastricly administered before MI];?5?atractylodes lactone ??? high dose group[atractylodes lactone ????60 mg/kg?intragastricly administered before MI];?6?atractylodes lactone ??? post-treatment group[atractylodes lactone ????60 mg/kg?intragastricly administered following MI];?7?atractylodes lactone ??? pre-treatment group[atractylodes lactone ????60 mg/kg?intragastricly administered prior to MI];?8?atractylodes lactone ??? pre and post-treatment group[atractylodes lactone ????60 mg/kg?intragastricly administered before and after MI].All the groups were treated 7days before the LAD ligation model was build.Echocardiography was performed to evaluate cardiac function,and cardiac fibrosis was evaluated using Masson's Trichrome staining on day 7 post MI.Histopathological examination of the tissue sections was performed to grade inflammatory cell infiltration,and platelet inhibition was monitored by measuring thrombin-induced platelet aggregation.Results:Compared with the control group,the LVEF and LVFS values of the atractylodes lactone ??? group were significantly increased in a dose-dependent manner?P<0.05?.In groups receiving pretreatment atractylodes lactone ???,cardiac LVEF and LVFS improved significantly compared with that seen in the post treatment and control groups?P<0.05?.Compared with the control group,cardiac fibrosis decreased in atractylodes lactone ??? groups in a dose-dependent manner?P<0.05?.Cardiac fibrosis decreased in groups receiving pretreatment compared to that seen in the post treatment and control groups?P<0.05?.Compared with the control group,inflammatory cell infiltration decreased in atractylodes lactone ??? groups in a dose-dependent manner?P<0.05?.Decreased inflammatory cell infiltration was observed in the pretreatment group compared with that of the control group?P<0.05?.Thrombin-induced platelet aggregation was increased with exposure to H₂O₂.Thrombin_-induced platelet aggregation in the presence of H₂O₂ was significantly inhibited by atractylodes lactone ???.In ex vivo,thrombin_-induced platelet aggregation was also significantly inhibited by atractylodes lactone ???.Conclusions:Pretreatment with atractylodes lactone ??? improved cardiac function,reduced cardiac fibrosis,decreased inflammatory cell infiltration after myocardial infarction and inhibited oxidative stress induced platelet aggregation.