Effact Of Folic Acid On Myocardial Apoptosis During Coxsackievirus B3 Infection Of Pregnant Rats In Heart Of Offspring

Objective: To investigate the effects of oral folic acid on myocardial apoptosis in an experimental model of coxsackievirus B3 (CV B3) infection of pregnant rats in heart of offspring.Method: Wistar rats were randomly divided into four groups: normal control; folic acid; CVB3; folic acid+ CVB3. Female rats in each group copulated with narmal male rats. The rats in normal control group were fed laboratory chow and given water ad labium. The folic acid group received folic acid fodder. In CVB3 group, CVB3 was injected by intraperitoneal injection for 5 days. In folic acid+ CVB3 group, CVB3 was injected by intraperitoneal injection for 5 days and fed with folic acid fodder. After natural childbirth neonatal heart were taken and stored in liquid nitrogen. Myocardial pathological section observed neonatal rat myocardial injury. Myocardial apoptosis was quantitated using tunel assay. RT-PCR and Western blot to observe apoptosis associated proteins.Results: Totally 40 included animals, three were died and one was aborted in CV B3 group; one rat produced two neonate rats in stillbirth; one rat was died in folic acid+ CVB3 group; 35 neonate rats were involved in the result analysis. In pregnant rats injected with CVB3, the myocardial cell injury was significantly in neonatal rats, under optical microscopy. Compared to the normal control group, significant increases in apoptosis were observed in group CVB3 (p<0.01), after oral folic acid the situation alleviated. An increase in Bax, Caspase-3 mRNA and protein levels were detected in CVB3 group compared with folic acid+ CVB3 group (p<0.05). The expression levels of Bcl-2 mRNA and protein levels were increased in folic acid+ CVB3 group compared with CVB3 group (p<0.01).Conclusions: Folic acid supplementation can effectively inhibit neonate rat myocardial cell apoptosis in the rats injected with CVB3. It can up-regulate the expression of Bcl-2 mRNA and protein, down-regulate the expression of Bax and Caspase-3 mRNA and protein, supply a path for protection neonate rat myocardial cell.