Abstract:Myocardial infarction is one of the leading causes of death in patients with coronary heart disease worldwide. In the early stage of acute myocardial infarction, percutaneous coronary intervention, coronary artery bypass grafting, drugs and other treatment means can restore the blood supply of ischemic myocardial tissue, save the dying myocardium and reduce the mortality rate of patients. However, after the interruption of myocardial blood supply and the restoration of blood supply within a certain period of time, the original ischemic myocardium may suffer more serious damage than that of ischemia. This phenomenon is called myocardial ischemia-reperfusion injury (MIRI), and its mechanism has not been fully elucidated. In this paper, the research progress of MIRI mechanism in recent years is reviewed, and the pathophysiological mechanism of MIRI is expounded, which will help to develop new therapeutic interventions and provide help for clinical treatment of myocardial infarction.

Abstract:Aim To explore the effect of salvia magnesium lithospermate B (MLB) on myocardial ischemia-reperfusion (IR)-induced cells programmed necrosis and its mechanism. Methods Myocardial infarction model was established by occlusion of the left anterior descending coronary artery in rats. After ischemia 1 h and reperfusion for 3 h, myocardial IR injury model was established. Rats were randomly divided into 7 groups:normal control group, sham operation group, IR group, MLB low dose (10 mg/kg)＋IR group, MLB high dose (30 mg/kg)＋IR group, necrostatin-1 (Nec-1; 3 mg/kg)＋IR group and solvent (normal saline)＋IR group (n＝6~8). Myocardial infarct area was detected by triphenyltetrazolium chloride staining. HE staining was used to observe the morphological changes of myocardial tissue. Serum creatine kinase (CK) activity was measured by spectrophotometry. The expression levels of programmed necrosis associated protein receptor interacting protein kinase 1 (RIPK1) and RIPK3 were detected by Western blot. Results High dose of MLB could significantly reduce the myocardial infarct size and CK release, and improve the myocardial tissue structure of IR rats, with the inhibition of RIPK1 and RIPK3 protein expression, which were better than the positive control drug Nec-1. Conclusion MLB has the function of resisting myocardial cell programmed necrosis, and its mechanism is related to the inhibition of RIPK1 and RIPK3 protein expressions.