Expression And Localization Of Group IIa Phospholipase A2 In Rats' Aorta, Myocardium And Visceral Adipose Tissue

BackgroudCoronary heart disease(CHD) is one of the most critical diseases that threaten human being.Many risk factors such as obesity , hyperlipidemia, diabetes,hypertetension and smoking have been intervened,but the incidence of CHD is still very high.Presently,the research about the mechanism of CHD has been a hot field all over the word.Since Ross initiatively suggested that atherosclerosis is a chronic inflammatiory disease,the theory has been amended and accepted by most scholars.Recently a clinical research discovered that the serum level of sPLA2 is significantly increased in CHD patients,and influences the stability of plaques.sPLA2 may predict independently the risk and prognosis of CHD. The deeply research on sPLA2 will shed new light on the cause,mechanism,diagnosis and therapy of CHD.0bjectiveTo investigate the expression and localization of group IIa secretory phospholipase A2(sPLA2 IIa) in atherosclerosis(AS)model rat s'aorta,myocardium and visceral adipose tissue(VAT); to study the effect of simvastatin on sPLA2 IIa.MethodsHealthy male Wistar rats were randomly divided into 3 groups (n=10 each):control group,model group,and simvastatin group(5 mg·kg-1·d -1 per gavage).The rats of model group and simvastatin group were feeded with high cholesterol diet.At the end of 8 weeks, sPLA2 IIa were observed by immunocytochemistry.Result1. sPLA2 IIa was present in smooth muscle cell and plaque of aorta.In contrast, sPLA2-IIa expression in aorta was much higher in model group than in controls(P <0.01), expression of the enzyme in aorta was significantly decreased in simvastatin group compared to model group(P<0.01).2. sPLA2 IIa was present in nucleus and cytoplasm of myocardium,the expression of sPLA2 IIa was significantly increased in model group compared to control group(P<0.01),and its expression was much lower in simvastatin group than in model group(P<0.01).3. sPLA2 IIa was present around lipid vacuole in adipocyte, no significant changes were found in levels of this enzyme among three groups.ConclusionsMyocardium and VAT maybe another two important sources of sPLA2-IIa. This result supports the hypothesis that sPLA2-IIa may play a significant role in the pathogenesis of AS. Simvastatin could relieve the process of AS by decreasing the expression level of sPLA2-IIa in myocardium and aorta .