Dexmedetomidine inhibits lipopolysaccharide-induced inflammatory response in hippocampal astrocytes in vitro

Neuroinflammation mediated by astrocytes has been implicated in neurodegenerative diseases. Meanwhile, dexmedetomidine (DEX) has potent anti-inflammatory properties. The present study aimed to assess the effects of DEX on proinflammatory mediator production and release in astrocytes after lipopolysaccharide (LPS) induction. Cultured astrocytes, derived from hippocampi of 4-day-old rats, were treated with DEX at 0.1, 1, 10, and 100 mu M, respectively, in the presence or absence of LPS (1 mu g/ml). Then, mRNA and protein levels of the proinflammatory cytokines TNF-alpha, IL-6 and IL-1 beta were measured. The protein levels of I kappa B-alpha were also assessed. DEX at 0.1 mu M or 1 mu M did not affect the production of proinflammatory mediators. However, higher DEX levels (10 and 100 mu M) significantly decreased the amounts of TNF-alpha, IL-6, and IL-1 beta, both at the mRNA and protein levels, and increased the protein levels of I kappa B-alpha. These findings indicate that DEX inhibits neuroinflammation by interfering with NF-kappa B signaling, and may constitute a potential therapeutic agent for protecting patients from neuroinflammation associated diseases.