Protective effect of salidroside on streptozotocin-induced diabetic nephropathy by inhibiting oxidative stress and inflammation in rats via the Akt/GSK-3 beta signalling pathway

Context Salidroside (SAL), one of the major glycosides isolated from the roots of Rhodiola rosea L. (Crassulaceae), has anti-inflammatory, antioxidant, and antidiabetic properties. Objective Our study assessed whether SAL exerts a protective effect on streptozotocin (STZ)-induced diabetic nephropathy (DN) in rats via the Akt/GSK-3 beta signalling pathway. Materials and methods Adult male Wistar rats were divided into three groups (n = 8): normal control, DN + vehicle, and DN + SAL. SAL (50 mg/kg/day, oral) was administered for 8 weeks. Biochemical and histopathologic examinations were performed to evaluate the therapeutic effects of SAL on oxidative stress, inflammation, renal function, and apoptosis. Results SAL induced rats demonstrated ameliorated levels of FBG (20.53 +/- 0.72 mmol/L vs. 26.02 +/- 1.44 mmol/L), urine albumin excretion (27.00 +/- 1.46 mmol/L vs. 41.00 +/- 1.59 mmol/L), blood urea nitrogen (14.42 +/- 0.70 mmol/L vs. 17.77 +/- 0.72 mmol/L), and serum creatinine (112.80 +/- 6.98 mmol/L vs. 159.00 +/- 3.81 mmol/L) compared to normal control rats, along with the alleviation of renal pathologic changes by improving the irregular shape of glomeruli tissues. Biochemical analysis showed that SAL-treated animals displayed suppressed levels of serum inflammatory cytokines and kidney oxidative stress markers and attenuated apoptotic characteristics. Moreover, it increased the phosphorylation levels of Akt and GSK-3 beta in kidneys. Discussion and conclusion The present study validated the involvement of the Akt/GSK-3 beta signalling pathway in renal improvement. These findings can form the basis to investigate the protective effect of SAL in DN in clinical trials.