Sevoflurane preconditioning ameliorates lipopolysaccharide-induced cognitive impairment in mice

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Author(s)

    • SATOMOTO Maiko Satomoto Maiko
    • Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan|Present address: Department of Anesthesiology, Graduate School of Medicine, Nagoya University, 65 Tsurumai, Showa-ku, Nagoya-shi, Aichi 466-8550, Japan
    • SUN Zhongliang Sun Zhongliang
    • Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
    • ADACHI Yushi U. Adachi Yushi U.
    • Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
    • MAKITA Koshi Makita Koshi
    • Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan

Abstract

<p>Systemic inflammation induces brain neuronal inflammation, in turn causing acute cognitive disorders. Furthermore, neuronal inflammation is one cause of postoperative cognitive disorder (POCD) and delirium. However, no sufficiently established pharmacological treatment is available for neurocognitive inflammation. This study evaluated the possible neuroprotective effects of preconditioning with sevoflurane anesthesia on cognition and neuroinflammatory changes in an animal model of lipopolysaccharide (LPS)-induced systemic inflammation. Adult mice were randomly divided into (1) control, (2) 2% sevoflurane preconditioning for 1 h, (3) intraperitoneal 5 mg/kg LPS injection, and (4) 2% sevoflurane preconditioning for 1 h + LPS injection groups. At 24 h after 5 mg/kg LPS injection, microglial activation based on ionized calcium-binding adapter molecule 1 (Iba-1) expression in the hippocampus was determined using immunostaining and immunoblotting. IL-1β and IL-6 immunoblotting were used as inflammation markers, and β-site of amyloid precursor protein cleaving enzyme 1 (BACE1) immunoblotting was performed to evaluate amyloid β-protein (Aβ) accumulation. Long-term cognitive impairment was evaluated using fear conditioning tests. Intraperitoneal LPS increased levels of Iba-1 (150%), inflammation markers (160%), and Aβ accumulation (350%), and sevoflurane preconditioning suppressed these increases. Systemic LPS caused learning deficits. Sevoflurane also maintained long-term memory in mice receiving LPS injection. Sevoflurane preconditioning prevented long-term memory impairment in the mouse model administered systemic LPS by decreasing excessive microglial activation, inflammation, and Aβ accumulation. This study supports the hypothesis that sevoflurane preconditioning might also be beneficial for neuronal inflammation. Sevoflurane might be beneficial for reducing delirium and POCD.</p>

Journal

  • Experimental Animals

    Experimental Animals 67(2), 193-200, 2018

    Japanese Association for Laboratory Animal Science

Codes

  • NII Article ID (NAID)
    130006733608
  • NII NACSIS-CAT ID (NCID)
    AA11032321
  • Text Lang
    ENG
  • ISSN
    1341-1357
  • NDL Article ID
    028961654
  • NDL Call No.
    Z54-H752
  • Data Source
    NDL  J-STAGE 
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