血管生成因子在糖尿病大鼠心肌组织的表达

 目的：检测糖尿病大鼠心肌组织中血管生成因子的表达。方法：选择雄性SD大鼠一次性腹腔注射链脲佐菌素制造1型糖尿病模型，糖尿病成功诱导后12周，运用MPA心功能分析系统评估心功能改变，Masson染色计算心肌胶原容积分数（collagen volume fraction，CVF），CD31免疫组织化学法测定心肌毛细血管并计算心肌毛细血管/心肌细胞比值（capillary/myocyte,C/M），Western blotting检测血管内皮生成因子（VEGF）、血管生成素1（angiopoietin-1，Ang-1）、血管生成素2（angiopoietin-2，Ang-2）和内皮抑素(endostatin) 在心肌组织中的表达。结果：与正常对照组比较，糖尿病大鼠左心室舒张末期压力(LVEDP)明显增高(P<001)，而左心室压力上升最大速率(+dp／dtmax)和左心室压力下降最大速率(-dp／dtmax)均明显下降（P<0.05）；心肌C/M比值、 VEGF和Ang-1表达明显减少（P<0.05）；而心肌CVF含量和endostatin表达显著增高（P<0.05）,但Ang-2表达无明显差异。结论：VEGF和Ang-1在糖尿病大鼠心肌组织表达下调，endostatin表达显著上调，可能是糖尿病心肌病发生的重要机制。

Expression of angiogenic factors in myocardial tissue of diabetic rats

AIM：To observe the expression of angiogenesis factors in the myocardial tissue of streptozotocin-induced diabetic rats. METHODS：The diabetic rat model was induced by intraperitoneal injection of streptozotocin. After 12 weeks, the cardiac function was measured by MPA cardiac function analysis system. The myocardial collagen volume fraction (CVF) was assessed by Masson staining. The capillary vessels was quantified as the ratio of capillary to myocyte (C/M) using CD31 immunostaining. The expression levels of vascular endothelial growth factor (VEGF), angiopoietin (Ang)-1, endostatin and Ang-2 were observed by Western blotting. RESULTS：Compared with normal control group, the left ventricular end-diastolic pressure (LVEDP) was evidently increased (P<0.01), but left ventricular pressure rise maximum rate (+dp／dtmax)， left ventricular pressure decrease maximum rate (-dp／dtmax) and the ratio of capillary/myocyte (C/M) were significantly decreased (P<0.05). The CVF and the expression level of endostatin were significantly increased, whereas the expression levels of VEGF and Ang-1 evidently decreased (both P<0.05) in diabetic rats. However, no marked difference in the expression of Ang-2 between the 2 groups was observed (P>0.05). CONCLUSION：Imbalances between the angiogenic factors (VEGF and Ang-1) and anti-angiogenic factors (endostatin) may play an important role in the pathogenesis of diabetic cardiomyopathy.