Abstract: AIM: To observe the effect of activation of melanocortin 4 receptor (MC4R) against sepsis induced renal injury and analyze the related mechanism.METHODS: Twenty four male SD rats were divided into 4 groups: Sham group, Sham+Ro27-3225 (the activator of MC4R) group, CLP group and CLP+Ro27-3225 group. CLP model was established by cecal ligation and puncture operation. Serum creatine (CRE), blood urea nitrogen (BUN) levels were measured and renal structural changes were observed by HE staining 24 h after CLP and NF-κB P65 expression in kidney tubules was measured by immunohistochemical method.The mRNA expression of NF-κB in kidney was determined by RT-PCR.RESULTS: Compared with Sham group, the levels of CRE and BUN were significantly increased (P<0.01), renal corpuscle was congested and wrinkled, capsular space was enlarged accompanying with epithelial cell swelling and necrosis. The expressions of NF-κB P65 protein and NF-κB mRNA level were increased (P<0.01). Compare with CLP group,the levels of CRE and BUN were decreased (P<0.01) in CLP+Ro27-3225 group, the damage of renal corpuscle and tubule was attenuated. The expression of NF-κB P65 protein and NF-κB mRNA level were decreased (P<0.01).CONCLUSION: Sepsis induced renal injury in rat CLP model,Activation of MC4R attenuated renal injury, which may be associated with decreasing NF-κB expression and reducing inflammatory reaction.

Key words: Sepsis, Renal injury, Melanocortin 4 receptor, NF-κB, Rat