Sevoflurane alleviates liver ischemia reperfusion injury through inactivation of the TRAF6/NF-κB signaling pathway

Purpose: To evaluate the role and mechanism of action sevoflurane in liver ischemia reperfusion injury.Methods: Rats were pretreated with then underwent followed by to establish an animal model injury. Pathological changes tissues investigated hematoxylin eosin (H & E) staining, serum levels alanine aminotransferase (ALT) aspartate (AST) determined using a chemistryanalyzer. ELISA was used determine myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), IL-6, superoxide (SOD), malonaldehyde (MDA), catalase (CAT), glutathione (GSH).Results: tissue, including sinusoidal congestion, vacuole formation, infiltration inflammatory cells lymphocytes, identified rats post-ischemia In addition, ALT AST increased following However, administration ameliorated pathological damage decreased ALTand induced reperfusion. Pro- cytokines, such as MPO, TNF-α, IL- 1β, IL-6 upregulated injury, this upregulation reversed administration. Sevoflurane also attenuated reperfusion-induced increase MDA decrease SOD, CAT, GSH. Ischemia reperfusionrepressed IκBα protein expression promoted TNF receptor associated factor 6 (TRAF6), phospho (p)-IκBα, p-p65 tissue. effect on IκBα, TRAF6, p-IκBα, p-65 expression.Conclusion: reduced injury bysuppressing response oxidative stress through inactivation TRAF6/NF-κB pathway.