Renoprotection of Danshen Injection on streptozotocin-induced diabetic rats, associated with tubular function and...

Danshen Injection, the aqueous extracts of Radix Salvia miltiorrhiza (S. miltiorrhiza), is one of the most commonly used traditional Chinese herbs in chronic renal failure treatment. In present study, the mechanism of the renoprotective effect of Danshen Injection was analyzed on streptozocin (STZ)-induced diabetic rats.

Diabetic experimental model was established in male Sprague-Dawley (SD) rats by intraperitoneal injection of STZ. Rats with blood glucose concentration of higher than 300 mg/dl were intraperitoneally administered with Danshen Injection at a dose of 0.78 ml/kgday. The blood glucose, 24h urinary protein excretion, serum creatinine (sCr), blood urea nitrogen (BUN), advanced glycation end products (AGEs), lipid peroxide (LPO), antioxidant enzyme of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), transforming growth factor-β1 (TGF-β1), and histomorphological changes in kidney of diabetic rats were analyzed during the course of Danshen Injection administration, as well as the tubular function index of albumin reabsorption of fluorescein isothiocyanate labeled bovine serum albumin (FITC-BSA).

The intraperitoneal administration of Danshen Injection could ameliorate the physiological dysfunctions of increased 24h urinary protein excretion((48.21 ± 8.04)%), sCr((39.4 ± 3.7)%), and BUN((43.37 ± 6.74)%), alleviate the ultrastructural abnormalities of hypertrophy, matrix expansion, and fibrosis in glomerulus, decrease the TGF-β1 expression, AGEs and LPO accumulation, and increase the activity of SOD and GSH-Px in kidney of diabetic rats, but did not significantly influence the blood glucose. Besides these, the Danshen Injection administration also partly restored the decrease of megalin expression in tubules and reabsorptive function of FITC-BSA, in diabetic rats.

The renoprotection of Danshen Injection on diabetic rats was associated with the preservation of tubular function and structure from the hyperglycemia induced toxicities of inappropriate cytokines secretion, oxidative stress, advanced glycation stress, and megalin expression deletion.