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目的 :探讨Ⅳ型胶原酶 (MMP2 及MMP9)在糖尿病大鼠肺组织表达的变化及蛋白激酶C(PKC)的作用。方法 :STZ腹腔注射制作糖尿病大鼠模型 ,4周后观察肺组织的病理改变 ,免疫组化方法检测MMP2 及MMP9在糖尿病大鼠肺组织表达的变化 ,采用改良的Takay法测定PKC活性 ,蛋白质免疫印迹分析 (Western -blot)及免疫组化方法检测TGF - β1表达含量的变化。结果 :DM大鼠 4周后肺泡间隔及毛细血管壁增厚 ,肺间质胶原成分增多 ,肺组织PKC活性增强 ,TGF - β1表达增多 ,MMP2 及MMP9表达下降。结论 :在糖尿病大鼠肺组织高糖环境下 ,PKC被激活导致TGF - β1表达增高 ,MMP2 、MMP9表达下降 ,引起细胞外基质 (ECM )合成降解失调 ,可能参与了糖尿病肺部并发症的发生及发展。
Objective: To investigate the changes of type Ⅳ collagenase (MMP2 and MMP9) in lung tissue and the role of protein kinase C (PKC) in diabetic rats. Methods: The model of diabetic rats was established by intraperitoneal injection of STZ. The pathological changes of lung tissue were observed after 4 weeks. The expressions of MMP2 and MMP9 in lung tissues of diabetic rats were detected by immunohistochemistry. The PKC activity and protein immunostimulation Western blotting and immunohistochemistry were used to detect the expression of TGF - β1. Results: After 4 weeks, the alveolar septum and capillary wall thickening, the interstitial collagen composition increased, the activity of PKC in lung tissue increased, the expression of TGF - β1 increased and the expression of MMP2 and MMP9 decreased in DM rats. CONCLUSION: PKC is activated in high glucose of lung tissue of diabetic rats, which leads to the increase of TGF - β1 expression, the decrease of MMP2 and MMP9 expression, and the degeneration of extracellular matrix (ECM) synthesis, which may be involved in the development of diabetic pulmonary complications And development.