Fish oils protects against cecal ligation and puncture‑induced septic acute kidney injury via the regulation of inflammation, oxidative stress and apoptosis.

Abstract

Septic acute kidney injury (AKI) is usually caused by sepsis. ω3 fatty acid has been reported to suppress sepsis-induced organ dysfunction to a certain degree. The present study aimed to investigate the effects of ω3 fatty acid in septic renal injury. Sprague Dawley rats were used to establish a cecal ligation and puncture (CLP) model in order to mimic the development of septic injury. The rats were treated with dexamethasone and fish oils (FOs) for 4 days prior to CLP. Alterations in the morphology of the tissues, the renal function and the induction of inflammation, oxidative stress and apoptosis were evaluated. The effects of FOs on nuclear factor-κB (NF-κB), JAK2/STAT3 and p38-MAPK were determined. The rats of the CLP model group exhibited low survival rates and increased expression of serum creatine, blood urea nitrogen, neutrophil gelatinase-associated lipocalin, kidney injury molecule-1 and of proinflammatory cytokines. In addition, the levels of the markers of oxidative injury and apoptosis were increased. The induction of renal injury was notably reversed by administration of dexamethasone and FOs. The expression levels of the protein markers involved in inflammation and apoptosis were measured and the results indicated that FOs inhibited JAK/STAT3 and p-38MAPK signaling, while they concomitantly increased the expression of NF-κB. The present study highlighted that FOs improve CLP-induced mortality and renal injury by inhibiting inflammation, oxidative stress and apoptosis.