4种不同污染源气体颗粒物及柯萨奇病毒B组3型对大鼠心肌细胞自噬和凋亡的影响

摘要

目的 观察LC3、LC3-II/LC3-I比值、Nrf2和Bcl2在柯萨奇病毒B组3型(coxsackievirus group B tyype 3,CV-B3)感染后引起的心肌炎和4种不同污染源气体颗粒物滴入气管后引起的SD大鼠心肌损害的不同变化,来探讨这些病理条件下心肌细胞自噬与抗凋亡、抗心肌损害作用机制.方法 将成年SD大鼠随机分为CV-B3感染组(20只)、汽车尾气组(20只)、煤烟组(20只)、燃烧秸秆组(20只)、大气组(20只)和对照组(20只);于实验12 h、48 h、5 d、10 d Western blot法检测大鼠LC3和Bcl2及Nrf2的表达.结果 前3组大鼠以上指标均表达上调,CV-B3组出现的早,峰值高,恢复快,汽车尾气组大鼠上述指标出现晚,幅度低,煤烟组大鼠以上指标出现更晚,但变化幅度高于汽车尾气组、低于CV-B3组,汽车尾气组和煤烟组第10天Bcl2和Nrf2仍轻度增高;大气组大鼠48 h以上指标出现了短暂的上调表达,第5天恢复正常,秸秆组和对照组大鼠以上指标始终未出现明显变化.结论 CV-B3诱导的急性病毒性心肌炎和汽车尾气、煤烟、大气颗粒物诱导的心肌损害的SD大鼠通过自噬激活、凋亡抑制和抗氧化机制来完成心肌细胞的的代谢、更新、修复、抗损伤的全过程.%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.