Nesfatin-1 ameliorates sepsis-induced remote organ injury: The role of oxidant-antioxidant status and neutrophils

Abstract

Purpose: Protective effects of nesfatin-1 was studied in sepsis-induced injury ofremote organs.Methods: Male rats were randomly divided as control and sepsis (cecal ligationperforation)groups, treated with either saline or nesfatin-1 (10 μg/kg). At 16 hfollowing surgery, samples of brain, kidney, liver and lung tissues were removedand myeloperoxidase (MPO) activity, glutathione (GSH), catalase (CAT), superoxidedismutase (SOD) and malondialdehyde (MDA) levels were measured in thesetissues.Results: In saline-treated septic rats, elevated MDA and MPO activities wereaccompanied with depleted CAT, SOD and GSH levels in the brain, kidney, liverand lung tissues, implicating extensive oxidative damage in all remote organs.Nesfatin-1 reduced MDA levels (brain, lung) and MPO activities (brain, kidney),and preserved antioxidant GSH (brain, lung), CAT (brain) and SOD (kidney) levels.Severe hepatocyte degeneration, neuronal damage, glomerulotubular degenerationand alveolar disturbance in saline-treated septic rats were replaced with regular tissuemorphologies in nesfatin-1-treated rats.Conclusion: Nesfatin-1 alleviates oxidative damage by enhancing endogenousantioxidant systems and inhibiting recruitment of neutrophils, suggesting thatnesfatin-1 may be have a potential therapeutic impact on the treatment of septicshock to reduce subsequent remote organ failure.