Salidroside protect renal function against inflammation and oxidative stress by NF-κB p65/NLRP3 pathway signaling in streptozocin induced diabetic nephropathy mice

Inflammation and oxidative stress have been reported to be a common product of many pathways that are involved in the pathogenesis of diabetic nephropathy. Salidroside, the major active compound in Rhodiola, provide multiple biological activities and has protective effects for alleviating diabetic renal dysfunction. However, the involved molecular mechanism was still not clarified well. In this study, we intended to explore the protective effects and further mechanism of salidroside in STZ-induced diabetic mice. Biochemical analysis was processed to investigate the anti-inflammatory effects and antioxidative effects in serum and kidney homogenate. Thus, the results showed that salidroside effectively reduced the level of blood glucose and GSP, ameliorated the renal function and kidney fibrosis in STZ-induced DN mice. STZ induced inflammation and oxidative stress in mice, which aggravated renal injury. Salidroside also suppressed the expression of proinflammatory factors (including IL-1, IL-1β, TNF-α) and the decreased MDA level, but increased the level of CAT, GSH-Px and SOD activity in STZ-induced mice. In mechanism, salidroside inhibited the expression of NF-κB p65 and NLRP3 pathway related proteins in vivo. Our findings suggest that salidroside improved renal inflammation and oxidative stress by inhibiting p65 and NLRP3 expression in STZ-induced diabetic mice. Our study provides a new potential treatment on diabetic nephropathy.