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目的：检测初发糖尿病大鼠肾小球蛋白激酶Ｃ（ｐｒｏｔｅｉｎ ｋｉｎａｓｅ Ｃ，ＰＫＣ）活性变化，以推断ＰＫＣ活性变化在肾内血流动力学改变中所起的作用。 方法：用链脲菌素制备糖尿病大鼠实验模型，在糖尿病发病２ 周后，分离肾小球，提取纯化胞浆及胞膜蛋白，利用γ３２ＰＡＴＰ 底物磷酸化的方法检测胞浆及胞膜ＰＫＣ活性。同时测量血、尿肌酐，计算内生肌酐清除率。 结果：糖尿病大鼠表现出明显的肾小球高滤过及肾脏肥大现象，此时细胞内总的ＰＫＣ 活性与对照组无显著性差异，胞浆ＰＫＣ活性略有下降，胞膜ＰＫＣ 活性明显增高，膜结合ＰＫＣ 百分比显著增加。表明胞膜ＰＫＣ活性的增高来源于其自胞浆向胞膜的转移，即初发糖尿病状态肾小球ＰＫＣ 被激活。 结论：链脲菌素糖尿病大鼠初发糖尿病阶段肾小球ＰＫＣ 即被激活，激活的ＰＫＣ通过参与多种血管活性物质的释放、离子通道的调节构成细胞内重要的信息网络系统，在糖尿病早期肾内血流动力学改变中发挥着重要的调控作用。
OBJECTIVE: To detect the changes of protein kinase C (PKC) activity in primary diabetic rats in order to deduce the role of changes in PKC activity in intrarenal hemodynamic changes. Methods: Streptozotocin was used to prepare diabetic rat model. After 2 weeks of diabetic onset, glomeruli were isolated and the purified cytoplasmic and cytoplasmic proteins were extracted. The cytoplasm and cells were detected by γ-32PATP substrate phosphorylation Membrane PKC activity. Simultaneous measurement of blood and urine creatinine, calculation of endogenous creatinine clearance. Results: The diabetic rats showed obvious glomerular hyperfiltration and renal hypertrophy. At this time, the total intracellular PKC activity was not significantly different from the control group, the cytoplasmic PKC activity decreased slightly, and the membrane PKC activity was significantly increased , The percentage of membrane-bound PKC increased significantly. The results showed that the increase of cell membrane PKC activity originated from the transfer from cytoplasm to cell membrane, that is, the initial diabetic state glomerular PKC was activated. CONCLUSION: PKC is activated in streptozotocin-induced diabetic rats during initial stage of diabetes mellitus. Activating PKC is involved in the release of many vasoactive substances. Regulation of ion channels constitutes an important intracellular information network system. In the early stage of diabetes Renal hemodynamic changes play an important regulatory role.