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目的:观测糖尿病大鼠肺组织转化生长因子蛋白激酶C(PKC)、转化生长因子β1(TGF-β1)、纤连蛋白(FN)活性的变化,探讨糖尿病大鼠肺纤维化的发病机制。方法:将实验大鼠分为对照组和糖尿病组,并于第8周采用免疫组化方法测定PKC、TGF-β1、FN在DM大鼠肺组织表达变化。结果:与对照组比较,糖尿病组大鼠肺组织中的PKC、TGF-β1、FN表达增多、活性增强。结论:链脲菌素糖尿病大鼠肺组织信号传导系统PKC-TGF-β1被激活,可引起FN表达增多,从而引起肺损伤。
Objective: To observe the changes of protein kinase C (PKC), transforming growth factor β1 (TGF-β1) and fibronectin (FN) in lung tissue of diabetic rats and to explore the pathogenesis of pulmonary fibrosis in diabetic rats. Methods: The experimental rats were divided into control group and diabetic group. The expression of PKC, TGF-β1 and FN in the lungs of DM rats were measured by immunohistochemistry in the 8th week. Results: Compared with the control group, the expression of PKC, TGF-β1 and FN in the lung tissue of diabetic rats increased and the activity increased. CONCLUSIONS: Streptozotocin-induced diabetic rat lung signal transduction system PKC-TGF-β1 is activated, which can cause the increase of FN expression and cause lung injury.