KDM2B regulates inflammation and oxidative stress of sepsis via targeting NF‐κB and AP‐1 pathways

Abstract Backgrounds The kidney is an easily affected organ with sepsis which a main underlying cause of acute injury (AKI). Histone‐modifying lysine‐specific demethylase 2B (KDM2B) involved in numerous pathological processes, such as cell senescence and tumor development. However, the role KDM2B sepsis‐induced AKI unclear. Objects To investigate on viability, inflammation oxidative stress sepsis‐associated AKI, signaling pathways. Methods An model vitro was established through lipopolysaccharide (LPS)‐induction HK‐2 cells. Western blots were performed to evaluate expression KDM2B, cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), p65, c‐Jun c‐Fos, well p65 phosphorylation. Cell viability measured using CCK‐8 kit. ELISA analyze production layered double hydroxide (LDH), necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐18, vascular adhesion molecule‐1 (VCAM‐1), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), H O . qPCR used transcription level TNF‐α, IL‐1β, VCAM‐1. Results knockdown alleviated LPS‐induced cytotoxicity, decreased LDH release, improved viability. reduced concentration inflammation‐related molecules including VCAM‐1, inhibited their transcription. Moreover, promoted quantity SOD GSH, while declined MDA, , COX2, iNOS. Further, played by activating nuclear κB (NF‐κB) activator protein 1 (AP‐1) Conclusion via inhibiting NF‐κB AP‐1 pathways, indicating may be promising therapeutic target for treatment AKI.