Oridonin relieves renal damage of diabetic rats through modulation of oxidative stress and lipid metabolism

Objective To investigate the protective effect and mechanism of oridonin on kidney of diabetic rats.Methods SD rats were randomly divided into three groups (n=8 per group) as follows:normal group (NC), diabetic mellitus group (DM), diabetic mellitus treated with oridonin group (DO). The rat diabetic model was established by intraperitoneal injection of STZ once. Oridonin was administered by gavage to the rats of DO group at a dose of 10 mg/kg/day for 8 weeks. The rats in NC group and DM group were treated with equal volume of normal saline. The animals were sacrificed after 8 weeks of treatment with oridonin. The 24-h urinary protein, serum creatinine (SCr), blood urea nitrogen (BUN), triglyceride (TG), total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), and the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) in renal tissues were determined. Western blotting and RT-PCR were used to detect the protein and mRNA expression of SOD. PAS staining was used to observe the pathological changes of renal tissues.Results As compared with NC group, DM group had significantly increased proteinuria, SCr, BUN, TG, TC and LDL, and decreased HDL. The content of MDA was increased but the activity of SOD and GSH-Px were decreased in renal tissues in DM group (P < 0.05). The protein and mRNA expression of SOD was decreased in renal tissues in DM group (P < 0.05). Oridonin treatment could reverse the renal function and renal histopathological changes, decrease the content of MDA, and increase the activity of SOD and GSH-Px (P < 0.05). The protein and mRNA expression of SOD was also up-regulated in renal tissues of rats treated with oridonin. And the levels of TG, TC and LDL were decreased, and the level of HDL was increased in plasma under the treatment of oridonin (P < 0.05).Conclusions Oridonin relieves renal damage of diabetic rats through modulation of oxidative stress and lipid metabolism.