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目的研究糖尿病大鼠不同病程心肌纤维化及其相关病理的变化。方法2003-12～2004-06在中国医科大学附属第一医院进行了糖尿病心肌病纤维化病理的如下实验研究:(1)制造糖尿病大鼠心肌模型随机分组;(2)氯胺T法测定羟脯氨酸表达,代表心肌胶原总表达。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D(λ);(3)心肌病理改变的光镜和透射电镜观察。结果(1)糖尿病病程6个月组心肌胶原总表达明显高于病程3个月以内组(P<0.01)。病程3个月之后CollagenⅠ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)。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,有糖原沉积现象。结论CollagenⅠ呈现持续性增加是糖尿病鼠心肌纤维化的主要原因。TGF-β1参与了心肌纤维化发生的早期过程。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 fibrosis and its related pathology in different course of diabetic rats. Methods The following experimental studies on the pathogenesis of diabetic cardiomyopathy were performed in the First Affiliated Hospital of China Medical University from December 2003 to June 2004: (1) Cardiac model of diabetic rats was randomly divided into groups; (2) Chloramine T Proline expression, representing the total expression of myocardial collagen. The mean integral optical density D (λ) of collagen Ⅰ, collagen α, α-actin and TGF-β1 were determined by immunohistochemical staining. (3) Pathological changes were observed by light and transmission electron microscopy. Results (1) The total expression of cardiac collagen in the 6-month diabetic group was significantly higher than that in the 3-month group (P <0.01). After 3 months, the expression of CollagenⅠwas significantly increased compared with healthy mice (P <0.01). The expression of α-actin protein was significantly lower than that of healthy mice (P <0.01). 3 months after the course of myocardial cell nuclear rupture, mitochondria swelling, fuzzy, intercalated disc discontinuity, glycogen deposition phenomenon. Conclusions Collagen Ⅰ is the main cause of myocardial fibrosis in diabetic rats. TGF-β1 is involved in the early course of myocardial fibrosis. Glycogen deposition and decreased expression of myocardial actin is the pathological basis of diabetic cardiomyopathy.