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.

Disruption of Kidney–Immune System Crosstalk in Sepsis with Acute Kidney Injury: Lessons Learned from Animal Models and Their Application to Human Health

“…The rIPC can attenuate production of inflammatory cytokines and reduce apoptosis in CLP mice; this effect is dependent on the activity of HIF1α and its downstream target, mIR-21 [18]. Similar findings of apoptosis of renal cells can be seen using TUNEL staining in rat models of CLP, where they are also accompanied by histological findings of glomerular atrophy, renal capsule dilation, tubular damage and epithelial cell necrosis [19]. Despite the above findings, it is generally accepted that there is not a large amount of cell death (necrotic or programmed) in sepsis-induced AKI in comparison to other types of AKI; that damage is instead driven by inflammation, disruptions to microcirculatory flow, and metabolic perturbations in response to injury [20].…”

The Inflammatory Response Induced by RELMβ Upregulates IL-8 and IL-1β Expression in Bronchial Epithelial Cells in COPD

“…There is increasing evidence that the p38 MAPK signaling pathway is involved in inflammatory effects. 21 , 22 To further analyze the potential mechanism by which RELMβ regulates the p38 MAPK signaling pathway, we treated the 16HBE cell line with the p38 MAPK signaling pathway inhibitor sb203580 for two hours. We analyzed the expression of phosphorylated p38 MAPK and the inflammatory factors IL-8 and IL-1β.…”

Tofacitinib protects intestinal epithelial cells against oxygen‑glucose deprivation/reoxygenation injury by inhibiting the JAK/STAT3 signaling pathway

“…By inactivating JAK/STAT3 signaling, dexmedetomidine was shown to inhibit the apoptosis of astrocytes induced by OGD/R ( 44 ). Fish oils have also been found to provide protection against cecal ligation and puncture-induced septic acute kidney injury by regulating inflammation, oxidative stress and apoptosis by suppressing JAK/STAT3 signaling ( 45 ). The present study suggests that Tofa can dose-dependently downregulate the phosphorylation and therefore activation of JAK1, JAK2 and STAT3 in IEC-6 cells under OGD/R conditions.…”