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目的通过观察过氧化物酶体增殖物激活型受体γ(PPARγ)与血管紧张素Ⅱ(AngⅡ)在糖尿病心肌纤维化模型大鼠心肌细胞及微血管中表达情况,初步探讨PPARγ在糖尿病心肌纤维化中的作用。方法雄性Wistar大鼠27只,随机分为①糖尿病组(n=15),给予大鼠腹腔内注射链佐菌素(STZ)65 mg/kg以制备糖尿病心肌纤维化大鼠模型;②正常对照组(n=12)。均给与标准饲料喂养5个月,糖尿病组大鼠成功建模并最终存活11只。采用放射免疫法测定各组血浆AngⅡ水平;心肌组织HE染色及Masson染色观察心肌细胞、胶原分布形态,测定胶原容量及微血管密度;采用免疫组织化学法测定AngⅡ及PPARγ在心肌细胞及微血管中表达。结果糖尿病组大鼠血浆AngⅡ水平明显高于正常对照组(P<0.05);糖尿病组心肌内胶原组织明显增多,微血管密度降低,胶原容量明显高于对照组(P均<0.05);镜下可见,糖尿病组心肌组织微血管内皮细胞及心肌细胞中PPARγ的大量表达,均明显高于正常对照组(P<0.05);AngⅡ在糖尿病组心肌细胞中的表达明显增高(P<0.05),而两组内皮细胞中的表达无差异(P>0.05)。结论糖尿病心肌纤维化大鼠心肌细胞和微血管内皮细胞中PPAR表达均明显增强,提示PPARγ可能在糖尿病心肌纤维化中发挥重要作用。
Objective To observe the expression of peroxisome proliferator-activated receptor γ (PPARγ) and angiotensin Ⅱ (AngⅡ) in cardiomyocytes and microvessels of diabetic rat with myocardial fibrosis, and to investigate the role of PPARγ in diabetic myocardial fibrosis In the role. Methods Twenty-seven male Wistar rats were randomly divided into ① diabetic group (n = 15), and streptozotocin (STZ) was given intraperitoneally to rats at a dose of 65 mg / kg to prepare diabetic rat model of myocardial fibrosis. ② Normal control Group (n = 12). All rats were fed with standard diet for 5 months. Rats in the diabetic group were successfully modeled and eventually 11 survived. The levels of plasma AngⅡ in each group were determined by radioimmunoassay. The distribution of myocardial cells and collagen was observed by HE staining and Masson staining. The collagen capacity and microvessel density were measured. The expression of AngⅡand PPARγ in cardiomyocytes and microvessels were detected by immunohistochemistry. Results The level of plasma AngⅡ in diabetic rats was significantly higher than that in normal controls (P <0.05). The collagen content in myocardium of diabetic rats was significantly increased, the density of microvessels was decreased and the collagen capacity was significantly higher than that of the control rats (all P <0.05) (P <0.05). The expression of AngⅡ in cardiomyocytes in diabetic group was significantly higher than that in normal control group (P <0.05), while the expression of PPARγ in cardiomyocytes of diabetic group was significantly higher than that in normal control group There was no difference in the expression of endothelial cells (P> 0.05). Conclusion The expression of PPAR in myocardial cells and microvascular endothelial cells of diabetic rats with myocardial fibrosis was significantly increased, suggesting that PPARγ may play an important role in diabetic myocardial fibrosis.