Effects of carvedilol on cardiomyocyte apoptosis in autoimmune myocarditis in mice

Objective To observe the effects of carvedilol on the expression of Bcl-2, Bax and Fas in autoimmune myocarditis (AM). Methods A total of 60 inbred male BALB/C mice 4-5 weeks of age were divided at random into 3 groups as follows: AM group (n=20), carvedilol group (n=20) and control group (n=20). The mice were sacrificed after gathering blood specimens by taking out the eyeballs and hearts tissue. The histological and ultrastructural changes were observed under light microscope and electron microscope. The concentrations of cardiac troponin I (cTn I) were detected by chemiluminescence immunoassay (CLIA). Immunohistochemistry (IHC) was performed to analyze the contents of Bcl-2, Bax and Fas, TUNEL to detect the apoptotic index in myocardial cells. Results There were large number of lymphocyte and monocyte infiltrates under light microscope and karyopyknosis and chromatin gathered along the nuclear membrane under electron microscope in AM group. There were no inflammations and chromatin gathering in group C. Compared with control group, the Bcl-2, Bax and Fas protein expression significantly elevated in AM group (23.48±2.24 vs. 6.64±1.60, 26.15±2.02 vs. 5.09±0.85, 21.22±3.62 vs. 5.86±1.37, P<0.01). The histopathologic scores(2.60±0.31 vs. 2.02±0.26, P<0.05)and karyopyknosis of carvedilol group decreased as compared with AM group. The Bcl-2, Bax and Fas protein expression (17.13±1.94 vs. 23.48±2.24, 17.66±2.62 vs. 26.15±2.02, 16.79±2.83 vs. 21.22±3.62, P<0.05), AI [(16.61±4.67)% vs.(24.51±4.70)%, P<0.05] and contents of cTnI [(1.878±0.48) ng/ml vs. (1.102±0.23) ng/ml, P<0.05] also decreased in carvedilol group compared with AM group. Conclusion Carvedilol could protect against AM by alleviating cardiomyocyte apoptosis. Key words: Myocarditis; Apoptosis; Beta-Adrenergic antagonists