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Published on: July 25, 2022
Dexmedetomidine attenuates lipopolysaccharide-induced proinflammatory response in primary microglia
Mian Peng1, Yan-Lin Wang, Cheng-Yao Wang
1Department of Anesthesiology, Zhongnan Hospital of Wuhan University, Wuhan, China. pm751101@yahoo.com.cn
Background:
Neuroinflammation mediated by microglia has been implicated in delirium. Suppression of microglial activation may therefore contribute to alleviate delirium. It has been reported that dexmedetomidine (DEX) has a potent anti-inflammatory property. In the present study, we investigated the effects of DEX on the production of proinflammatory mediators in lipopolysaccharide-stimulated microglia.
Materials And Methods:
The concentrations of DEX were chosen to correspond to 1, 10, and 100 times of clinically relevant concentration (i.e., 1, 10, and 100ng/mL). The levels of proinflammatory mediators, such as inducible nitric oxide synthase or nitric oxide, prostaglandin E(2), interleukin 1β, and tumor necrosis factor α, were measured.
Results:
DEX at 1ng/mL did not affect the production of proinflammatory mediators. DEX at 10 and 100ng/mL significantly inhibited the release of nitric oxide, prostaglandin E(2), interleukin 1β, and tumor necrosis factor α and the expression of inducible nitric oxide synthase messenger RNA.
Conclusions:
These results suggest that DEX is a potent suppressor of lipopolysaccharide-induced inflammation in activated microglia and may be a potential therapeutic agent for the treatment of intensive care unit delirium.
