论文部分内容阅读
目的:观察卡维地洛对病毒性心肌炎小鼠的保护作用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只作总体对照。观察各组小鼠的心肌组织病理学改变、cTn-I水平及心肌组织磷酸化p38MAPK含量的变化。结果:美托洛尔、卡维地洛干预后,小鼠心肌组织病理改变减轻,cTn-I水平、心肌磷酸化p38MAPK含量均下降,卡维地洛干预后上述指标下降更加显著。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p38MAPK通路活化,减轻病毒性心肌炎引起的心肌损伤。
Objective: To observe the protective effect of carvedilol on viral myocarditis in mice and explore its possible mechanism. Methods: A total of 188 clean grade inbred male BALB / c mice aged 4-6 weeks were randomly divided into 4 groups. Myocarditis control group (C group), metoprolol intervention group (M group), carvedilol intervention group (K group) each 60, blank control group (B group) 8 as a control. The changes of myocardial histopathology, cTn-I level and phosphorylated p38MAPK content in myocardium were observed in each group. Results: After the intervention of metoprolol and carvedilol, the pathological changes of myocardium in mice were alleviated. The levels of cTn-I and phosphorylated p38MAPK in myocardium decreased. The carvedilol intervention decreased more obviously. CONCLUSION: Carvedilol may inhibit the activation of p38MAPK pathway and attenuate myocardial injury induced by viral myocarditis through the dual block of β1 and β2 adrenergic receptors.