Abstract: Objective To explore the activation and its role of JNK signal pathway in kidney of mice with lipopolysaccharide (LPS) induced acute kidney injury (AKI) . Methods Forty-eight male were randomly divided into control group and AKI group to measure the levels of blood urea nitrogen ( BUN ),serum creatinine ( Scr) and cystatin C(Cys C) respectively. The pathologic change to the kidney were detected by HE. Immunohistochemistry( IHC) and Western blot were applied to detected the expression of p-JNK and p-c-Jun respectively. Serum level of TNF-α and IL-1β was determined by ELISA. Results Compared with the control group, BUN, Scr and Cys C levels of the AKI group rose considerably after the injection and the pathological damages of their renal tissues showed a continual worsening trend. A weak expression of p-JNK and p-c-Jun on the renal tubule and glomerular mesangial region was detected. The expression and protein leval of p-JNK and p-c-Jun was up-regulated in AKI group compared with normal controls,which started to increase after 1 hours, peaked at 4 hours and decresed remarkably at 30 hours. Meanwhile, TNF-α and IL-1β levels in the blood also rose obviously and peaked at 4 hours after the injection followed by a gradual decrease. Conclusion JNK signal pathway may play an important role in the pathogenesis of AKI induced by LPS. Activation of JNK signal pathway could mediate the occurrence and development of AKI by triggering the expression of TNF-α and IL-1β.

Key words: Lipopolysaccharide acute kidney injury c-Jun amino-terminal kinase signal pathway