黄芩苷对糖尿病肾病大鼠肾功能及其抗氧化应激作用的研究

目的研究黄芩苷对糖尿病肾病(DN)大鼠肾功能的影响,并从抗氧化应激反应的角度探讨其作用机制。方法采用链尿佐菌素单次腹腔注射法造成DN大鼠模型,腹腔注射黄芩苷水溶液。6周后所有大鼠称体重、肾重,并计算肾指数;收集大鼠24h尿液,测尿微量蛋白值、尿肌酐值;一侧肾脏做电镜及病理形态学检查,另一侧肾脏匀浆后测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)活性。结果黄芩苷组尿微量蛋白含量明显减少,尿肌酐排泄量增加,与模型组比较差异有显著性(P<0.05);肾脏组织学观察显示,黄芩苷组肾小球基底膜较模型组明显变薄,系膜区细胞外基质(ECM)沉积减少,硬化的肾小球数量减少,肾小管上皮细胞水肿现象明显减轻,足细胞密度增加,足突融合现象减轻;黄芩苷组SOD活性升高,与模型组比较差别有统计学意义(P<0.05);黄芩苷组GSH-PX活性较模型组升高,但两者差别无统计学意义(P>0.05)。结论黄芩苷可减轻DN大鼠蛋白尿、提高尿肌酐排泄功能、减少肾脏ECM沉积,延缓DN的发展进程,其作用机制可能与提高肾脏抗氧化系统功能,从而减轻DN时肾脏局部氧化应激反应有关。

Effect of Baicalin on Renal Function in Diabetic Nephropathy Rats and Its Anti-oxidative Action

Objective To explore the effects of baicalin (Bai) on renal function of diabetic nephropathy (DN) rats and on the antioxigenic enzymes levels of actien mechanism. Methods DN rat model was established by one-dose intraperitoneal injection of streptozotocin. Six weeks after injection with baicalin into the abdominal cavity of DN rats,renal index was caculated,24-hour urine was gathered and microprotein content was measured,one kidney was used for morphological examination under electron microscope,and the other one was used to make homogenate for measuring the SOD and GSH-PX activities. A normal control group was also established at the same time. Results Microprotein in the urine of baicalin group was significantly decreased,and there was significant difference between this group and the model control group (P < 0.05);Renal tissue observation showed that glomerular basement membrane in the baicalin group was much thinner than that in the model group,and there was less extracellular matrix (ECM) deposit in the mesangial area,less edema in the epithelial cells of renal tubule;There was significant difference of SOD activity between the baicalin group and the model group (P < 0.05);GSH-PX activity in the baicalin group was higher than those in the model group,but the difference was insignificant (P > 0.05). Conclusion Baicalin can decrease urine protein in DN rats and ECM deposit in the kidney,and delay the development progress of DN. Its mechanism is probably related to the increase of antioxigenic function of the kidney.