黄芪甲苷对糖尿病肾病大鼠肾脏的保护作用及其机制

Protective effect of astragaloside IV on kidney of diabetic nephropathy rats

目的:观察黄芪甲苷(AS-IV)对糖尿病肾病(DN)肾脏的保护作用及其机制。方法:38只清洁级雄性SD大鼠分成正常组(10只)、模型组(14只)和AS-IV干预组(14只),用链脲佐菌素造模,成功后1周开始治疗,期间每4周动态观测血糖及尿微量白蛋白,治疗12周后处死大鼠取材及采血,取肾皮质行HE和Masson染色观察,并检测β1整合素、整合素连接激酶(ILK)和α-actinin-4的蛋白表达水平。结果:干预8周末AS-IV组血糖水平较模型组明显降低(P<0.01)。干预12周末AS-IV组与模型组相比,尿微量白蛋白明显下降(P<0.01),并使因造模引起的β1整合素、ILK和α-actinin-4表达水平的变化产生逆变(P<0.05)。与正常组比较,模型组的β1整合素、ILK和α-actinin-4表达水平均有明显差异(P<0.05)。结论:AS-IV对DN肾脏有明显保护作用,能降低血糖和尿白蛋白排泄量,改善足细胞黏附功能,从而延缓DN的进展。

AIM： To observe the protective effect of astragaloside IV （AS-IV） on the kidney of diabetic ne- phropathy （DN） rats and its mechanism. METHODS： Male SD rats （n = 38） were divided into normal group （n = 10）, model group （n = 14） and AS-IV intervention group （n = 14）. The rats in model group and intervention group were injec- ted with streptozotocin for inducing DN. One week after the success of modeling, the blood glucose and urinary microalbu- min were dynamically monitored every 4 weeks during the study. After treatment for 12 weeks, the rats were sacrificed, the blood samples and the renal cortex were collected. HE staining and Masson staining were applied for observing the patho- logical changes of the renal tissues. The protein levels of β1 integrin, integrin-linked kinase （ILK） and α-actinin-4 were also detected. RESULTS ： At the end of the 8th week, the glucose level in AS-IV intervention group was significantly low- er than that in model group （P 〈0.01）. After 12 weeks of treatment, compared with model group, the amount of urinary microalbumin in AS-IV intervention group was significantly decreased （P 〈 0.01 ）, and the inverse changes of the β1 inte- grin, ILK and α-actinin-4 expression in AS-IV intervention group were also observed （ P 〈 0.05 ）. Compared with normal group, the levels of β1 integrin, ILK and α-actinin-4 in model group were significantly different （P 〈 0.05 ）. CONCLU- SION： AS-IV has a protective effect on DN kidneys. AS-IV reduces blood glucose and urinary albumin excretion, improves the adhesion of podocytes and delays the development of DN.