病毒性扩张型心肌病小鼠IL-6测定及意义

目的建立病毒性扩张型心肌病（DCM）小鼠模型并测定其血清白介素（IL-6）含量，初步探讨IL-6在DCM小鼠的致病机制。方法40只4周龄雄性BALB／c小鼠随机分成DCM（扩张型心肌病）组和正常组，每组各20只。DCM组每月腹腔注射柯萨奇病毒B3（CVB3），6个月后建立DCM模型，取出小鼠心脏进行病理组织学观察，并采用酶联免疫吸附法（ELISA）检测DCM组及正常组小鼠血清IL-6表达水平。结果腹腔反复注射病毒6个月后，DCM组小鼠心脏稍有增大，但最大横径与正常组相比差异无统计学意义（P〉0．05），重量比正常组有所增加（P〈0．05），左室游离壁厚度显著变薄（P〈0．05）。DCM组小鼠血清IL-6水平（150．6±47．2）pg／ml，正常组为（82．9±63．1）pg／ml（P〈0．05）。结论反复腹腔注射CVB3病毒能成功建立DCM模型，IL-6表达水平在DCM时明显升高，可能参与了DCM的发病过程。

Expression of IL-6 in Viral Dilated Cardiomgopathy Mice

Objective To investigate IL-6 levels in coxsackievirus-induced dilated eardiomyopathy （DCM） mice and the underlying mechanism. Methods A total of 40 male BALB/c mice,4 weeks old,allocated 20 in the DCM group and 20 in the control group randomly. Mice in DCM group were peritoneally injected （PI）with eoxsackievirus B3 （CVB3/Nancy）monthly and sacrificed after 6 month. Left ventricle thickness,weight and transverse diameter of DCM mice hearts were measured,and IL-6 levels were detected by ELISA. Remits The hearts of mice in DCM group became larger after 6 month of PI with CVB3, but no difference in transverse diameter of hearts between DCM mice and the control （P 〉0.05） ,and the weight increased,left ventricle free wall thickness thinned in DCM group when compared with control group （ both P 〈 0.05）. IL-6 levels in DCM group were higher than the control （ 150. 6 ± 47.2） pg/ml vs （ 82.9 ± 63. 1 ） pg/ml ] （P 〈 0.05）. Conclusion DCM mice model could be induced by repeatly peritoneal injection with coxsackievirus B3. Expression of IL-6 increasing in DCM mice serum, which suggested that IL-6 may involved in DCM pathogenesis.