Objective: To study the correlation of the electrical remodeling of myocardial cellwith oxidative stresand inflammatory injury in animal modelwith dilated cardiomyopathy.Methods: Male New Zealand white rabbitwere selected aexperimental animaland divided into model group and control group, model group were made into animal modelwith dilated cardiomyopathy through eaintravenouinjection of adriamycin, and the control group received eaintravenouinjection of same dose of saline.Eighweeklater, the myocardial tissue wacollected to detecthe myocardial cell delay aftedepolarization (DADs) through the technique of unicell patch clamp, and radioimmunoprecipitation kitand enzyme-linked immunosorbenassay kitwere used to determine oxidative stresindexeand inflammatory reaction indexes.Results: The incidence of myocardial cell DADof animal model group wasignificantly highethan thaof control group, and ROS, MDA, AOPP, CHOP, GRP78, TLR4, NF-kB, IL-1β, IL-6 and TNF-α levelin myocardial tissue were significantly highethan those of control group;ROS, MDA, AOPP, CHOP, GRP78, TLR4, NF-kB, IL-1β, IL-6 and TNF-α levelin myocardial tissue of DADanimalin model group were significantly highethan those of non-DADanimals.Conclusions: Adriamycin-induced dilated cardiomyopathy can lead to myocardial cell delay aftedepolarization through oxidative stresand inflammatory injury.%目的:研究扩张型心肌病动物模型心肌细胞电重构与氧化应激及炎症性损伤的相关性.方法:选择雄性新西兰大白兔作为实验动物并分为模型组和对照组,模型组采用阿霉素耳缘静脉注射的方式建立扩张型心肌病动物模型,对照组给予等剂量生理盐水耳缘静脉注射.8周后收集心肌组织并通过单细胞膜片钳技术测定心肌细胞晚期后除极(DADs)情况,采用放射免疫沉淀试剂盒和酶联免疫吸附试剂盒测定氧化应激反应指标、炎症反应指标.结果:模型组动物心肌细胞DADs的发生率显著高于对照组,心肌组织中ROS、MDA、AOPP、CHOP、GRP78、TLR4、NF-kB、IL-1β、IL-6、TNF-α的含量均显著高于对照组;模型组中DADs动物心肌组织中ROS、MDA、AOPP、CHOP、GRP78、TLR4、NF-kB、IL-1β、IL-6、TNF-α的含量均显著高于非DADs动物.结论:阿霉素所致扩张型心肌病能够通过氧化应激及炎症性损伤来造成心肌细胞晚期后除极.
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