Dexmedetomidine protects gastric mucosal epithelial cells against ischemia/reperfusion-induced apoptosis by inhibiting HMGB1-mediated inflammation and oxidative stress

Purpose: To investigate the role of dexmedetomidine in gastric ischemia/reperfusion injury using mucosal epithelial cell (GES-1) model.
 Methods: GES-1 were subjected to oxygen-glucose deprivation conditions, followed by increasing concentrations (0.5, 1.0, or 1.5 μM) for 4 h reoxygenation. Cell viability and apoptosis determined 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide flow cytometry, respectively. Oxidative stress inflammation analyzed enzyme-linked immunosorbent assay (ELISA).
 Results: Oxygen-glucose conditions induced cytotoxicity decreasing apoptosis. Dexmedetomidine treatment significantly increased hypoxia/reoxygenation-induced (p < 0.01) but reduced also attenuated increase malondialdehyde myeloperoxidase, decrease superoxide dismutase glutathione GES-1. Moreover, upregulated tumor necrosis factor-α, interleukin (IL)-1β, IL-18 was downregulated treatment. enhanced IL-10 levels inhibited proinflammatory factor production 0.01). High-mobility group box 1 (HMGB1) protein hypoxia/reoxygenation decreased dexmedetomidine. HMGB1 over-expression dexmedetomidine-induced apoptosis, oxidative stress, 
 Conclusion: protects against ischemia/reperfusion-induced inflammation, inhibiting HMGB1, thus providing a potential strategy treating injury.
 Keywords: Dexmedetomidine; cells; Ischemia/reperfusion; Apoptosis; Inflammation; stress;