Anti-Inflammatory Action of Dexmedetomidine on Human Microglial Cells

• Published in: International journal of molecular sciences Vol. 23; no. 17; p. 10096
• Main Authors: Yamazaki, Sho, Yamaguchi, Keisuke, Someya, Akimasa, Nagaoka, Isao, Hayashida, Masakazu
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 03-09-2022; MDPI
• Subjects: Adrenergic receptors; Anesthesia; anti-inflammatory action; Chemokines; Cognition & reasoning; cytokine; Cytokines; Delirium; dexmedetomidine; Hospital costs; Inflammation; Interleukin 6; Interleukin 8; Kinases; Lipopolysaccharides; MAP kinase; Microglia; Microglial cells; Mortality; Neurodegeneration; NF-κB protein; Pathogenesis; Phosphorylation; signaling molecule
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms231710096

Neuroinflammation, where inflammatory cytokines are produced in excess, contributes to the pathogenesis of delirium. Microglial cells play a central role in neuroinflammation by producing and releasing inflammatory cytokines in response to infection, tissue damage and neurodegeneration. Dexmedetomidine (DEX) is a sedative, which reduces the incidence of delirium. Thus, we hypothesized that DEX may alleviate delirium by exhibiting anti-inflammatory action on microglia. In the present study, we investigated the anti-inflammatory action of DEX on human microglial HMC3 cells. The results indicated that DEX partially suppressed the IL-6 and IL-8 production by lipopolysaccharide (LPS)-stimulated HMC3 cells as well as the phosphorylation of p38 MAPK and IκB and the translocation of NF-κB. Furthermore, DEX substantially suppressed IL-6 and IL-8 production by unstimulated HMC3 cells as wells as the phosphorylation of p38 MAPK and IκB and the translocation of NF-κB. These observations suggest that DEX exhibits anti-inflammatory action on not only LPS-stimulated but also unstimulated microglial cells via the suppression of inflammatory signaling and cytokine production.