Abstract
Our study aimed to explore the molecular mechanisms involved in the improvement of postoperative cognitive dysfunction (POCD) by dexmedetomidine (DEX). BV2 microglia cells were cultured under normal condition, DEX exposure (0.1 μg/mL), and lipopolysacchride (LPS) treatment (0.1 μg/mL) or with pretreatment of DEX before LPS incubation. For BV2 microglia cells, LPS induced markedly increased release of pro-inflammatory cytokines (interleukin [IL]-1β, IL-6, and tumor necrosis factor-alpha [TNF-α]) and expressions of Toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB), while DEX pretreatment inhibited the LPS-induced production of pro-inflammatory cytokines and expressions of TLR4 and NF-κB. The spatial memory function was impaired in the aged mice following partial hepatectomy since the percentage of time spent in the target quadrant and the number of crossings over the former platform location were reduced. Pretreatment of DEX may attenuate neuroinflammation and improve POCD in aged mice through inhibiting the TLR4-NF-κB signaling pathway in the hippocampus.