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作 者:罗永姣[1] 邓晖[1] 李双杰[2] 杜九中[1]
机构地区:[1]南华大学第一附属医院儿科,湖南省衡阳市421001 [2]湖南省儿童医院感染科,湖南省长沙市410000
出 处:《中国动脉硬化杂志》2010年第6期353-356,共4页Chinese Journal of Arteriosclerosis
基 金:国家自然科学基金资助项目(NO30271665)
摘 要:目的探讨单核细胞趋化蛋白1在病毒性心肌炎中的作用及黄芪甲甙干预后的变化。方法 55只雄性Balb/c小鼠随机分为正常对照组(n=10)、模型对照组(n=15)、低剂量干预组(n=15)及高剂量干预组(n=15),后3组小鼠经腹腔接种0.1mL柯萨奇病毒B3建立病毒性心肌炎模型,低剂量干预组和高剂量干预组于病毒接种后当天分别以0.01g/L、0.09g/L黄芪甲甙0.1mL灌胃,正常对照组和模型对照组均以羧甲基纤维素钠溶液灌胃,第15天处死全部存活小鼠,心脏石蜡切片HE染色计算病理积分,免疫组织化学染色检测单核细胞趋化蛋白1蛋白表达,逆转录-聚合酶链反应检测单核细胞趋化蛋白1mRNA表达。结果正常对照组、模型对照组、低剂量干预组及高剂量干预组死亡率分别为0、46.7%、40.0%、13.3.0%,高剂量干预组死亡率明显低于模型对照组和低剂量干预组(P<0.05)。模型对照组心肌单核细胞趋化蛋白1mRNA及蛋白表达水平均明显高于正常对照组(P<0.01),高剂量干预组病理积分及单核细胞趋化蛋白1mRNA、蛋白表达量较模型对照组、低剂量干预组显著降低(P<0.05或0.01)。结论单核细胞趋化蛋白1参与病毒性心肌炎发病过程,黄芪甲甙对病毒性心肌炎的治疗作用可能与其抑制单核细胞趋化蛋白1表达有关。Aim To explore the effect of monocyte chemoattractant protein-1 ( MCP-1 ) in viral myocarditis ( VMC ) and the change of MCP-1 after astragaloside intervention. Methods Fifty-five male 4-week-old Balb/c mice were randomly divided into 4 groups: normal control group (n = 10) , model control group In = 15 ), low-dose intervention group ( n = 15 ) and high-dose intervention group ( n = 15 ). Mice in the latter three groups were inoculated with 0.1 mL coxsackie B3 virus intraperitoneally. Then, mice in low-dose and high-dose intervention groups were treated with 0.01 g/L and 0.09 g/L astragaloside solution, respectively. Mice in normal control group and model control group were treated with carboxymethycellulose solution. All mice were killed on day 15. Histological cross sections of heart were stained with hematoxylin-eosin and myocardial histopathologic scores were counted under optical microscope. The expression levels of myocardial MCP-1 mRNA and protein were detected by RT-PCR and immunohistochemistry. Results The mor- tality was 0, 46.7%, 40.0% and 13.3% in normal control group, model control group, low-dose intervention group and high-dose intervention group respectively. Compared with model control group and low-dose intervention group, the mortality was significantly lower in high-dose intervention group ( P 〈 0.05 ). The expression levels of MCP-1 mRNA and pro- tein for model control group were markedly higher than those of normal control group ( P 〈 0.01 ). However, the expres- sion cevels of MCP-1 mRNA and protein and myocardial histopathologic scores in high-dose intervention group were decreased markedly compared with model control group and low-dose intervention group ( P 〈 0.05 or 0.01 ). Conclusion MCP-1 may participate in the pathogenesis of VMC. The therapeutic effect of Astragaloside on VMC is associated with inhibiting MCP-1 expression.
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