Effects of particulates in four different air pollution sources and coxsackie virus B3 on autophagy and apoptosis of cardiac myocytes in rats / 中华实验和临床病毒学杂志

ABSTRACT

Objective@#To observe the changes of LC3, lc3-Ⅱ/lc3-Ⅰ ratio, Nrf2 and Bcl2 in myocarditis induced by coxsackievirus group B type 3 (CV-B3) infection and myocardial damage in SD rats caused by particulate matter of four different pollution sources, and to further explore the mechanism of autophagy and apoptosis of myocardial cells and myocardial damage.@*Methods@#Adult SD rats were randomly divided into CV-B3 infection group (20 rats), automobile exhaust group (20 rats), coal smoke group (20 rats), burning straw group (20 rats), atmosphere group (20 rats) and control group (20 rats). The expressions of LC3, Bcl2 and Nrf2 in rats were detected by Western blot at 12 hours, 48 hours, 5 days and 10 days.@*Results@#In the first three groups of rats expression of LC3, Bcl2 and Nrf2 was upregulated, this was seen early in CV-B3 group, the peak was high, and recovery was fast; while in automobile exhaust group the above changes appeared later, the amplitude was low; in the coal smoke group rats the above changes appeared even later, but the amplitude of change was higher than that in automobile exhaust group, but lower than that of CV-B3 group. In automobile exhaust and coal smoke groups Bcl2 and Nrf2 expression was still slightly increased at day 10. After 48 hours, the above measurements in rats in the atmosphere group were temporarily up-regulated, and returned to normal on day 5. The above measurements of rats in the straw smoke and the control group did not show significant change.@*Conclusions@#In the SD rats with acute viral myocarditis induced by CV-B3 and myocardial damage induced by automobile exhaust, coal smoke and atmospheric particulate matter, the whole process of metabolism, renewal, repair and anti-damage activity of myocardial cells can be accomplished through autophagy activation, apoptosis inhibition and antioxidant mechanism.