Myocardial Cytosolic Phospholipase A2 Expression In Rats'model Of Acute Myocardial Infarction

BackgroudCoronary heart disease is not only a global health issue,but also a big catastrophic human disease, Incidence of which is increasing year by year. Acute myocardial infarction is the most critical form of coronary heart disease, At the same time,it is the common cause of emergency, hospital and death.Sensitive and specific biochemical markers such as cardiac troponin and creatine kinase MB fragment levels of the blood, along with acute ischemic clinical background, can be diagnosed as classic myocardial infarction.These biochemical markers may reflect myocardial ischemia, but could not explain the mechanism of ischemia. Therefore, seeking the mechanisms of ischemic myocardial injury and their associated factors in the acute myocardial infarction is particularly important.Cytosolic phospholipase A2 contain many kinds of enzymes,which can hydrolyze the phospholipase in the membrance into fatty acid and lysophosphatide.productions of these lipids not only act as the second messagers in the cell,but also metabalize into effective mediators in the inflammatory reaction. Recent studies indicate that cPLA2 is likely the major PLA2 that hydrolysis phospholipid and release lipid inflammatory mediators in the pathological conditions of acute myocardial cells, cPLA2 plays an important role in ischemia, hypoxia-induced organ. so an in-depth study of cPLA2 will further clarify pathology and pathophysiology of acute myocardial infarction,and provide new ideas for diagnosis and prevention.ObjectTo explore the role of cPLA2 in acute myocardial infarction(AMI) by observing the dynamc cPLA2 expression changes at mRNA and protein levels and determining creatine kinase isoenzyme (CK-MB) activity in the myocardial tissue and plasma and myocardial membrane phospholipids at different time pointsMethodsHealthy male SD rats were randomly divided into Sham and AMI group .The rats were killed according to different myocardial infarction time (0,1,2, 3, 6 and 12hours .cPLA2 expressions at protein and mRNA levels were detected by immunohistochemistry and RT-PCR respectively. It in different time points was detected in myocardial tissue and plasma CK-MB activity and myocardial membrane phospholipids.Results1. Compared to Sham group, cPLA2 mRNA level was upregulated in myocardium in AMI group and peaked at 2 hours after myocardial infarction.2. Positive cPLA2 protein staining was visualized in both Sham and AMI groups and significantly increased and peaked at 2 hours after AMI groups.3. A marked increase in CK-MB in plasma was found at the 3 hours after AMI, accompanied by a low ering of its content in myocardium. Mean while, cell membrane phospholipid contents were decreased at the 2 hours after AMI.4.Cell membrane phospholipid contents showed a remarkable relationship with changes in both cPLA2 expression and CK-MB activity. CK-MB activity Of myocardial tissue showed a remarkable relationship with changes in plasma CK-MB activityConclusionsThe up-regulation of cPLA2 expression may be responsible for myocardial lesion through aggravation of membrane phopholipid degradat ion. phospholipase A2;Membrane phospholipid;creatine kinase isoenzyme...