心肌胶原蛋白和肌动蛋白对糖尿病心肌病变的研究(英文)

Effect of cardiac muscle collagen and actin on myocardiopathological change of diabetes mellitus

目的研究糖尿病大鼠不同病程心肌胶原蛋白和骨架蛋白含量的变化,阐明两者对糖尿病心肌病变发生的作用。方法制造糖尿病大鼠心肌模型随机分组。氯胺T法测定羟脯氨酸含量,代表心肌胶原总含量。心肌免疫组织化学染色测定心肌胶原蛋白(CollagenI、CollagenIII)和心肌型α肌动蛋白(α-actin)及转化生长因子β1(TGF-β1)平均积分光密度(IOD)。心肌病理改变的光镜和透射电镜观察。结果糖尿病病程6个月组心肌胶原总含量明显高于病程3个月以内组(P <0.01)。病程3个月之后I型胶原蛋白表达伴随TGF-β1的表达开始较健康鼠明显增加(P <0.01)。α-actin蛋白表达较健康鼠明显减少(P <0.01)。糖尿病鼠心肌横切面可见粗大胶原纤维相互连接成网状,排列紊乱,分布不匀。心肌细胞心肌型α-actin蛋白分布不均匀,着色呈浅黄色,心肌纵切面可见α-actin蛋白表达主要分布于心肌肌膜处。病程3个月后大鼠心肌细胞核皱缩,线粒体肿胀、模糊,闰盘不连续,α-actin蛋白表达明显减少,有糖原沉积现象。结论Ⅰ型心肌胶原蛋白呈现持续性增加是糖尿病鼠心肌纤维化的主要原因。心肌细胞核皱缩,线粒体肿胀、模糊,闰盘不连续,糖原沉积和心肌型actin表达减少是糖尿病心肌病病理基础。

To investigate the content changes of myocardial collagenprotein and actin at different stages of diabetes mellitus(DM) rats. So as to illustrate that they play a role in myocardial changes of DM. Cardiac muscle model of DM rats was grouped randomly. The hydroxy proline contents were measured with the chloramine T method. The type I collagen, type Ⅲ collagen,transforming factor beta1 (TGF-beta1) and cardiac-type α-actin were determined by myocardial immunehistochemical stain. Myocardiopathological change were observed with light microscope and transmission electron microscope. The collagen contents of experimental rats increased much more obviously of one month group and six months group than those of three months group (P <0.01). The cardiac-type α-actin expression subsided obviously from three to six months (P <0.01). There were great difference in cardiac-type α-actin expression among the 1st, the 3rd and the 6th months (P <0.01) group. All in all, cardiac-type α-actin expression decreased along with the disease headway gradually. The myocardial mitochondria had already shown not distinct and out of order, the intercalated disk distorted, cracked and big gap, the cell nucleus were malformation, the cell nucleus and endoplasm had a large quantity of glucogenic accumulating phenomenon. [Conclusion] The increasing type I collagen proteins are the principal cause of myocardial fibrosis of diabetes mellitus. The expression of cardiac-type actin decrease in diabetes mellitus rats. The microscopic changes in pathology are the cell nucleus contracture, mitochondrial swollening with glycogen deposition.