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作 者:王丹[1] 褚茂平[1] 陈其[2] 姜建斌[2] 钱燕[1]
机构地区:[1]温州医学院附属第一医院儿科,325000 [2]温州医学院附属育英儿童医院心血管科
出 处:《浙江医学》2011年第4期529-532,共4页Zhejiang Medical Journal
基 金:基金项目:浙江省卫生厅资助项目(2004A070)
摘 要: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.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.
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