摘要
Object： To examine the effect of astragalus polysaccharide （APS） on kidney status and fibrosis indices of rats withdiabetic nephropathy. Methods： 72 male rats were randomly divided into three groups： negative control group （NC, n =24）; diabetic nephropathy model group （DNM, n = 24）; and diabetic nephropathy model with APS group （DNM ＋ APS,n = 24）. Rats of the DNM and DNM ＋ APS groups were subjected to both unilateral nephrectomy and administeredstreptozotocin （STZ） injection （65 mg/kg）. DNM ＋ APS group rats were administered 50 IU/kg/d APS by subcutaneousinjection from the first week after operation until death. The NC and DNM group rats were subcutaneously injected withan identical volume of physiological saline. At weeks 3, 8, and 13 after the operation, 6 rats from each group wererandomly sacrificed and blood was collected to measure serum creatinine and blood urea nitrogen. On the day beforesacrifice, the rats were placed in a metabolic cage for 24 h to collect urine. At week 14 after the operation, 6 rats fromeach group were randomly selected to measure body weight and kidney index. Blood was collected to measure bloodglucose. The kidneys were harvested to detect pathological changes by hematoxylin and eosin staining. Results：Histological assessment of DNM rats suggested damage symptoms as evidenced by hyperplasia of the glomerularmesangial matrix, atrophia of the kidney tubules, and thickening of the basement membrane. In contrast, STZ-induceddiabetic nephropathy rats treated with APS （50 IU/kg/d） showed significantly improved histological results, suggestingthat APS has beneficial effect on renal tissues in STZ-induced DNM rats. Our results also indicated that APS relievedrenal injury and effectively improved body weight in DNM rats. The ratio of kidney weight to body weight was reducedand the early stage of renal function damage was improved after APS treatment. In the later stages of the disease, the 24h urinary protein significantly decreased. Moreover, APS down-regulated TGF-β1 and α-SMA expression of the kidney.Conclusion： APS significantly improved renal tubular interstitial injury in DNM rats and the early stage of renalfunction damage. The mechanism may be related to downregulation of the expression of TGF-β1 and α-SMA whichdelays the progression of renal interstitial fibrosis in DNM rats.
