摘要
目的:研究糖尿病心肌细胞的结构变化及Ca2+调控蛋白基因表达的改变。方法:经大鼠尾静脉注射四氧嘧啶(40mg/kg)复制糖尿病大鼠模型,对照组注射生理盐水,分别于2、4、6周处死,取心尖部组织行普通光镜及透射电镜观察大鼠心肌结构的改变。应用逆转录-聚合酶反应技术以肌动蛋白为内参,测定钙离子调控蛋白基因表达的改变。结果:4周、6周大鼠的心脏/体重比显著大于正常对照组。电镜下糖尿病组大鼠心肌细胞的亚细胞器出现重构,表现为肌原纤维含量明显减少,排列紊乱,内质网扩张,线粒体变性等改变。6周的糖尿病组大鼠心肌肌浆网Ca2+-ATP酶的mRNA表达无明显变化,但磷酸受纳蛋白的mRNA表达显著高于对照组,1,4,5三磷酸肌醇受体2型,兰尼碱受体2型的mRNA表达显著低于对照组。结论:糖尿病大鼠心肌细胞的亚细胞器出现重构,肌浆网磷酸受纳蛋白的mRNA表达增加,RyR2、IP3R2的mRNA表达下降。
Objective： To investigate the ultrastructure of myocardium and gene expression of calcium handling proteins in diabetic rat heart. Methods： Diabetes was induced in male Sprague-Dawley rats by a single injection of alloxanm（40 mg/kg ） and the rats in control group were injected with normal saline. At the end of 2,4,6 weeks after the induction of diabetes, the animals were sacrificed. The expression of calcium handling proteins was detected by reverse transcription-polymerase chain reaction （RT-PCR） and actin mRNA was used as internalstandard. Heart tissue at the apex was obtained for light and electron microscope study. Results ： At the end of 4 and 6 weeks ,cardiosomatic ratio of diabetic rats was higher than that of control. Electron microscopy revealed a spectrum of subcellular remodeling in myocardium which was characterized by damaged myofibrils and mitochondria,dilated and swollen sarcoplasmic reticulum. Expression of phospholamban mRNAs was significantly increased,but 1,4,5-trisphosphate inositol receptor type 2, ryanodine receptor type 2 mRNAs were significantly decreased compared with those in the age-matched control rats. In contrast,the expression of sarco/endoplasmic reticulum Ca^2＋ -ATPase mRNAs was not affected. Conclusion： In diabetic rat heart,gene expression of calcium handling proteins was characterized by up-regulation of phospholamban and down-regulation of sarcoplasmic reticulum calcium release channel while electron microscopic analysis of myocardium revealed a spectrum of subcellular remodeling.
出处
《浙江大学学报（医学版）》
CAS
CSCD
2005年第5期454-458,共5页
Journal of Zhejiang University(Medical Sciences)
基金
国家教育部留学回国人员科研基金资助(1999-747)
