卡维地洛对病毒性心肌炎小鼠ERK1/2通路的影响

目的 观察卡维地洛对病毒性心肌炎小鼠心肌组织细胞外信号调节激酶（ERK1/2）信号通路的影响并探讨其可能的作用机制.方法 188只清洁级近交系4~6周龄雄性Balb/C小鼠随机分成4组.心肌炎对照组（C组）、美托洛尔干预组（M组）、卡维地洛干预组（K组）各60只,空白对照组（B组）8只做总体对照.观察各组小鼠各时间点（1、3、7和14d）的心肌组织病理学改变、血清cTnI水平、IL1β含量及心肌组织磷酸化ERK1/2含量的动态变化.结果 病程第1、3天,M组、K组心肌磷酸化ERK1/2水平低于C组（P＜0.01）,病程第14天,K组心肌磷酸化ERK1/2水平仍低于C组（P＜0.01）.病程第3、7天,M组、K组心肌组织炎症积分、血清cTnI和IL-1β水平低于C组（P＜0.05或0.01）,且K组上述水平下降更加显著（P＜0.01）.结论 卡维地洛可能通过β1、β2肾上腺素能受体双重阻滞作用,抑制ERK1/2信号通路活化,减轻病毒性心肌炎引起的心肌损伤.

Effects of carvedilol on signal pathway ERK1/2 in mice with myocarditis

Objective TO investigate the effects of carvedilol on signal pathway ERK1/2 in mJce with myocarditis. Methods A total of 188 inbred male Balb/C mice of 4-6 weeks were divided into 4 groups： myocarditis group （group C, n=60）, metoprolol treatment group （group M, n=60）, carvedilol treatment group （group K, n=60）, control group （group B, n=8）. Western Blot were performed to analyze the contents of phosphorylated ERK1/2 in myocardium, histopathlolgic changes of myocardium were ob- served. The concentrations of cardiac troponin I （cTn-I） were detected by chemiluminescene immunoassay （CLIA）. Results The value of myocardial phosphorylated ERK1/2 of group M and K was decreased on dl and d3, and also on d14 in group K. The levels of inflammation score, cTn-I and IL-1β were attenuated in group M and K on d3 and d7, and more markedly in group K. Conclusion Carvedilol may protect mice from viral myocarditis by inhibition of ERK1/2 signal transduction pathway through blockade of β1 and β2 adrenergic receptors.