卡维地洛对病毒性心肌炎小鼠的保护作用及其机制

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β1、β2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。

Effects of carvedilol on murine viral myocarditis

AIM: To observe the effects of carvedilol on murine viral myocarditis model. 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). Myocardial histopathololgic changes were observed. The concentrations of cardiac troponin I (cTn-I) were detected by chemiluminescence immunoassay (CLIA). Western blotting was performed to analyze the contents of phosphorylated p38MAPK in myocardium. RESULTS: Metropolol and carvedilol lightened myocardial histopathololgic changes at acute stage, decreased cTn-I concentrations and myocardial phosphorylated p38MAPK value compared with myocarditis group. Treatment with carvedilol was more effective than treated with metropolol on those indexes. CONCLUSION: Carvedilol protects against viral myocarditis by inhibition of p38MAPK signal transduction pathway through blockade of β_1 and β_2 adrenergic receptors.