Objective: Microglia have different phenotypic and functional states: M1 is associated with inflammatory responses, whereas M2 results in anti-inflammatory effects. The cellular state of microglia plays an important role in brain inflammation associating with many neuroinflammatory diseases. The purpose of this study was to detect the effect of dexmedetomidine (Dex) on inflammatory inhibition and microglial polarization in BV-2 cells.
Materials And Methods: Dex exerts anti-inflammatory effects in various experimental models. The BV-2 microglial cell line was treated with liposaccharide in the presence or absence of Dex. The M1 and M2 markers were evaluated by quantitative real-time PCR (qRT-PCR) and western blot.
Results: We found that Dex exerted a potent anti-inflammatory effect by reducing the expression of M1 marker genes such as tumor necrosis factor alpha (P < 0.05), interleukin-1β (IL-1β) (P < 0.001) and IL-6 (P < 0.001). Importantly, Dex improved the expression of microglia M2 markers arginase-1 (Arg-1) (P < 0.01), Flt3-interacting zinc finger protein 1 (Fizz-1) (P < 0.001) and CD206) (P < 0.001). Further, Dex enhanced the activation of Akt pathway.
Discussion: Our results indicated that Dex promotes microglia from the M1 phenotype to the M2 phenotype. Therefore, Dex may be a potential novel therapeutic drug for treating brain inflammation-associated diseases not only because of its anti-inflammatory property but also because it can remodel M1 phenotype microglia to M2 phenotype microglia.
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