[Effects and mechanism of salidroside on streptozotocin-induced mode rats of diabetic nephropathy].

OBJECTIVE: To investigate the effects and mechanism of salidroside(SAL) on model rats of diabetic nephropathy(DN). METHODS: Rats were divided into control, model, SAL(50 mg/kg), SAL(100 mg/kg) and SAL(200 mg/kg) groups. The rats beside in control group were injected with streptozotocin(STZ) combined with right nephrectomy. And rats in SAL(50, 100, 200 mg/kg) groups were received gavage with SAL(50, 100, 200 mg/kg). After 12 weeks, rats were sacrificed and kidneys were collected. HE staining was performed for renal injury, the concentrations of urine protein, urine creatine(Ucr), blood urea nitrogen(BUN), malondialdehyde(MDA), superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px) were measured by kits. Western blot was used to measure the protein levels of Collagen Ⅳ, fibronectin, E-cadherin, α-smooth muscle actin(α-SMA), N-cadherin, Smad2、Smad3, phosphorylated-Smad2(p-Smad2), p-Smad3 and transforming growth factor-ß1(TGF-ß1). RESULTS: Compared with control group, the renal injury of rats in model group was aggravated, the concentrations of urine protein, Ucr and BUN were elevated significantly, the apoptosis cells and positive cells of caspase-3 were increased; compared with model group, the renal injury of rats in SAL(100, 200 mg/kg) groups were alleviated markedly, the concentrations of urine protein, Ucr and BUN were reduced, the apoptosis cells and positive cells of caspase-3 were decreased notably. SAL(50 mg/kg) increased the concentration of SOD in DN model rats, SAL(100, 200 mg/kg) increased the concentrations of SOD and GSH-Px, decreased the level of MDA. Meanwhile, the inhibition of collagen Ⅳ, fibronrctin, α-SMA, and N-cadherin and the induction of E-cadherin in DN rats were induced by SAL(100, 200 mg/kg). In addition, SAL(100, 200 mg/kg) reduced the ratio of p-Smad2/Smad2, p-Smad3/Smad3 and the level of TGF-ß1(P<0.05 or P<0.01). CONCLUSION: SAL can inhibit renal fibrosis of STZ-induced DN model rats, and the mechanism may be related to inhibition of TGF-ß1/Smad pathway.