Objective: 

Nesfatin-1, an anorexigenic and anxiogenic peptide, was identified in 2006 in the adipose tissue, gastric mucosa, pancreatic b-cells and several brain areas. Recent studies have shown that nesfatin-1 has antiapoptotic and anti-inflammatory properties. The aim was to investigate the protective effects of nesfatin-1 against oxidative organ injury in sepsis.

Methods: 

Under anesthesia, sepsis was induced by cecal ligation-perforation method. Male Sprague-Dawley rats (n=24) were divided into sham-operated control, saline-treated sepsis and nesfatin-1 (10 mg/kg; i.p.) - treated sepsis groups. Rats were decapitated at the 16 h of surgery and liver, kidney, brain and lung samples were obtained for histological analysis and for the measurement of myeloperoxidase (MPO) activity and malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) levels. Values are compared by ANOVA.

Results: 

Compared to control group, sepsis resulted in significant decreases in GSH, SOD and CAT levels with increases in MDA levels and MPO activities (p<0.05–0.001), showing oxidative damage in all tissues of saline-treated rats. Treatment with nesfatin-1 alleviated sepsis-induced tissue damage, while MDA levels and MPO activities were reduced along with the preservation of the antioxidant GSH, CAT and SOD levels in all tissues (p<0.05). All histological data also support these findings.

Conclusions: 

The current results suggest the anti-inflammatory effects of nesfatin-1 in sepsis-induced oxidative damage by the augmentation of endogenous antioxidants and the inhibition of neutrophil recruitment. Thus, nesfatin-1 may be regarded as a potential therapeutic agent in the treatment of septic shock to reduce subsequent remote organ failure.