Influence of astragalus polysaccharide on kidney status and fibrosis indices of a rat model of streptozotocininduced diabetic nephropathy

Object: To examine the effect of astragalus polysaccharide (APS) on kidney status and fibrosis indices of rats with diabetic 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 administered streptozotocin (STZ) injection (65 mg/kg). DNM + APS group rats were administered 50 IU/kg/d APS by subcutaneous injection from the first week after operation until death. The NC and DNM group rats were subcutaneously injected with an identical volume of physiological saline. At weeks 3, 8, and 13 after the operation, 6 rats from each group were randomly sacrificed and blood was collected to measure serum creatinine and blood urea nitrogen. On the day before sacrifice, the rats were placed in a metabolic cage for 24 h to collect urine. At week 14 after the operation, 6 rats from each group were randomly selected to measure body weight and kidney index. Blood was collected to measure blood glucose. 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 glomerular mesangial matrix, atrophia of the kidney tubules, and thickening of the basement membrane. In contrast, STZinduced diabetic nephropathy rats treated with APS (50 IU/kg/d) showed significantly improved histological results, suggesting that APS has beneficial effect on renal tissues in STZinduced DNM rats. Our results also indicated that APS relieved renal injury and effectively improved body weight in DNM rats. The ratio of kidney weight to body weight was reduced and the early stage of renal function damage was improved after APS treatment. In the later stages of the disease, the 24 h urinary protein significantly decreased. Moreover, APS downregulated TGFβ1 and αSMA expression of the kidney. Conclusion: APS significantly improved renal tubular interstitial injury in DNM rats and the early stage of renal function damage. The mechanism may be related to downregulation of the expression of TGFβ1 and αSMA which delays the progression of renal interstitial fibrosis in DNM rats.