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 of remote organs. Methods: Male rats were randomly divided as control and sepsis (cecal ligation-perforation) groups, treated with either saline or nesfatin-1 (10 mu g/kg). At 16 h following surgery, samples of brain, kidney, liver and lung tissues were removed and myeloperoxidase (MPO) activity, glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA) levels were measured in these tissues. Results: In saline-treated septic rats, elevated MDA and MPO activities were accompanied with depleted CAT, SOD and GSH levels in the brain, kidney, liver and 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 degeneration and alveolar disturbance in saline-treated septic rats were replaced with regular tissue morphologies in nesfatin-1-treated rats. Conclusion: Nesfatin-1 alleviates oxidative damage by enhancing endogenous antioxidant systems and inhibiting recruitment of neutrophils, suggesting that nesfatin-1 may be have a potential therapeutic impact on the treatment of septic shock to reduce subsequent remote organ failure.