Dexmedetomidine reduces lipopolysaccharide induced neuroinflammation, sickness behavior, and anhedonia

Ching Hua Yeh, Liang Po Hsieh, Ming Chung Lin, Tsui Shan Wei, Hui Ching Lin, Chia Cheng Chang, Chung Hsi Hsing*

*此作品的通信作者

研究成果: Article同行評審

28 引文 斯高帕斯(Scopus)

摘要

Background Peripheral innate immune response may induce sickness behavior through activating microglia, excessive cytokines production, and neuroinflammation. Dexmedetomidine (Dex) has anti-inflammatory effect. We investigated the effects of Dex on lipopolysaccharide (LPS)induced neuroinflammation and sickness behavior in mice. Materials and methods BALB/c mice were intraperitoneally (i.p.) injected with Dex (50 ug/kg) or vehicle. One hour later, the mice were injected (i.p.) with Escherichia coli LPS (0.33 mg/kg) or saline (n = 6 in each group). We analyzed the food and water intake, body weight loss, and sucrose preference of the mice for 24h. We also determined microglia activation and cytokines expression in the brains of the mice. In vitro, we determine cytokines expression in LPS-treated BV-2 microglial cells with or without Dex treatment. Results In the Dex-pretreated mice, LPS-induced sickness behavior (anorexia, weight loss, and social withdrawal) were attenuated and microglial activation was lower than vehicle control. The mRNA expression of TNF-α, MCP-1, indoleamine 2, 3 dioxygenase (IDO), caspase-3, and iNOS were increased in the brain of LPS-challenged mice, which were reduced by Dex but not vehicle. Conclusion Dexmedetomidine diminished LPS-induced neuroinflammation in the mouse brain and modulated the cytokine-associated changes in sickness behavior.

原文English
文章編號e0191070
期刊PLoS ONE
13
發行號1
DOIs
出版狀態Published - 1月 2018

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