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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。
Objective To study the changes of myocardial collagen and skeletal protein in different stages of diabetic rats and to elucidate their roles in the development of diabetic cardiomyopathy. Methods Myocardial models of diabetic rats were randomly divided into groups. Chloramine T method for determination of hydroxyproline content, representing the total myocardial collagen content. Myocardial immunohistochemical staining was used to determine the average integral optical density (IOD) of Collagen I and α-actin and TGF-β1. Pathological changes of myocardium were observed with light microscope and transmission electron microscope. Results The total content of myocardial collagen in the 6-month diabetic group was significantly higher than that in the 3-month group (P <0.01). After 3 months of course of disease, type I collagen expression began to increase with the expression of TGF-β1 (P <0.01). α-actin protein expression was significantly reduced compared with healthy mice (P <0.01). Myocardial cross-section of diabetic rats showed thick collagen fibers connected to each other into a network, arranged in disorder, uneven distribution. Myocardial myocardial α-actin protein distribution uneven, pale yellow, myocardial longitudinal section shows α-actin protein expression mainly in the myocardium Department. 3 months after the course of myocardial cell nuclear ruffling, mitochondria swelling, fuzzy, intercalated disc discontinuity, α-actin protein was significantly reduced, the phenomenon of glycogen deposition. Conclusions The sustained increase of type Ⅰ myocardium collagen is the main reason of myocardial fibrosis in diabetic rats. Myocardial cell nuclear shrinkage, mitochondrial swelling, fuzzy, intercalated disc discontinuity, glycogen deposition and decreased expression of myocardial actin is the pathological basis of diabetic cardiomyopathy.