【摘要】 目的:探讨肝内胆汁淤积症(ICP)孕鼠的胎鼠心肌细胞缝隙连接蛋白43(Cx43)和缝隙连接蛋白45(Cx45)的表达。方法:应用雌、孕激素建立妊娠肝内胆汁淤积大鼠模型,透射电镜观察胎鼠心肌细胞闰盘超微结构,免疫组化、RT-PCR和Western Blot检测胎鼠心肌细胞Cx43和Cx45的表达。结果:(1)ICP组胎鼠心肌细胞闰盘结构部分模糊,缝隙连接消失;(2)免疫组化、RT-PCR和Western blot实验均发现,ICP组胎鼠心肌细胞Cx43蛋白表达显著下调,与正常组胎鼠比较,差异有极显著性,均P<0.01。(3)免疫组化、RT-PCR和Western blot实验均发现,ICP组胎鼠心肌细胞Cx45蛋白表达与正常组胎鼠比较差异无显著性,P>0.05。结论:ICP孕鼠的胎鼠心肌细胞缝隙连接超微结构发生改变,Cx43蛋白表达下调,缝隙连接通讯受到明显抑制,可能导致胎鼠发生心律失常和猝死。更多还原

【Abstract】 Objective:To investigate the expression of myocardium connexin43 and connexin45 in fetal rat of intrahepatic cholestasis of pregnancy(ICP).Methods:The animal model of ICP was induced by 17-α-Ethinylestradiol and Progesterone.Ultrastructural changes of intercalated disk of fetal rat myocardial cells(FRMCs) were observed by electromicroscope.Expression of connexin43 and connexin45 of FRMCs were observed by immunohistochemistry,RT-PCR and Western Blot.Results:(1)It showed vague ultrastructure in some parts of intercalated disk and disappeared gap junctions of FRMCs in Group ICP.(2)Expression of connexin43 by immunohistochemistry,RT-PCR and Western Blot was downregulated significantly in FRMCs of Group ICP when compared to control,P<0.01.(3)No obvious differences were found about the expression of connexin45 by immunohistochemistry,RT-PCR and Western Blot in FRMCs between Group ICP and control,P>0.05.Conclusion:It demonstrated that ultrastructural changes of gap junction,downregulation of connexin43 and inhibition of gap junction intercellular communication in FRMCs might contribute to fetal rat arrhythmia and sudden death in ICP.更多还原