A Study On The Correlation Between Calpain Mrna Expression And Cardiocyte Apoptosis In Acute Murine Coxsackievirus B3 Myocarditis

Objective To detect the expression of Calpain-1 and Calpain-2 mRNA and study its relationship with cardiocyte apoptosis in acute murine coxsackievirus B_3(CVB_3) myocarditis.Methods Balb/ c mice were single infected with CVB_3 to establish the experimental model of acute myocarditis.Meanwhile, drug(N-acetyl-Leu-Leu-Norleucinal,ALLN) intervention group(n=12) and vehicle control group(n= 10) were set.Normal controls(n=8) were prepared with same volume of Dulbecco's Modified Eagle Media(DMEM) without CVB_3.The cardiocyte apoptosis was detected through Terminal Deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling(TUNEL) method and the apoptosis rate of each slide was calculated.The expression level of Calpain-1 and Calpain-2 mRNA were determined by RT-PCR.Results Compared with the normal group and the vehicle control group,both the Calpain-1(P=0.02 and P=0.04) and Calpain-2(P<0.01 and P=0.02) mRNA expression level of the virus group were increased significantly followed by a significant apoptosis rate increase(both P values<0.01) respectively as well.No significant statistic difference was achieved between the normal control group and the vehicle control group as for both the Calpain-1(P>0.05) and Calpain-2(P>0.05) mRNA expression level and the cardiocyte apoptosis rate.The drug intervention group was significantly different with the normal control group(both P values<0.01) and the virus group(P=0.04 and P<0.01) respectively with regard to both the Calpain-1 and Calpain-2 mRNA expression level and the cardiocyte apoptosis rate(both P values<0.01).Calpain-1 and Calpain-2 mRNA expression level were significantly correlated with the cardiocyte apoptosis rate respectively. Conclusions Coxsackievirus B_3 participated in the onset of acute myocarditis via its activation effect on Calpain of the beart tissue,which caused pathologic damage through a certain mechanism correlated with cardiocyte apoptosis.