Objective:To explore the effect of asiatic acid(AA) on renal c-Jun N-terminal kinase(JNK) signaling pathway and podocyte in diabetic rats. Methods:Diabetic model was established by injection of streptozotocin. The diabetic rats were divided into two groups: diabetes mellitus group(DM group) and AA treated group (AA group). The normal non-diabetic rats were served as the control group (NC group). After eight weeks, the serum urea nitrogen (BUN), serum creatinine(SCR), the excretion of urinary albumin excretion rate (UAER), the blood glucose, the activity of superoxide dismutase(SOD) and the level of malonaldehyde(MDA) in renal cortex were detected. The structure of podocytes was observed by electron microscope. The expressions of p-JNK and JNK protein in kidney tissue of rats were examined by Western blot. The expression of nephrin protein in podocyte was examined by immunohistochemistry. Results:Compared with NC group, in DM group, the levels of BUN, SCR,UAER and blood glucose were significantly elevated(all P < 0.01); the level of MDA in renal cortex was significantly elevated(P < 0.05); the activity of SOD was significantly reduced(P < 0.05); the foot process width was increased, the glomerulus basement membrane was thickened, the mesenterium mass were increased; the expressions of p-JNK and JNK in kidney tissue were significantly increased(all P < 0.01); the nephrin expression was significantly reduced(P < 0.01). Compared with DM group, in AA group, the levels of BUN,SCR,UAER, and MDA in renal cortex were significantly reduced (all P < 0.05); the activity of SOD was significantly increase(P < 0.05); the abnormal structure of podocyte was obviously improved; the expressions of p-JNK and JNK were significantly reduced (all P < 0.05); the nephrin expression was significantly increased(P < 0.05). Conclusion: Asiatic acid may up-regulate the expression of nephrin in the podocyte of DM rats and inhibit the JNK signaling pathway activation showing the protective effect of diabetic nephropathy.