Protective role of dexmedetomidine in unmethylated CpG-induced inflammation responses in BV2 microglia cells
Unmethylated CpG DNA, as a stimulatory molecule, has potent pro-inflammatory effects in the central nervous system (CNS). Dexmedetomidine (DEX) has been confirmed to exert anti-inflammatory effects in CNS. Our study was aimed to explore the effects of DEX on tumor necrosis factor-α (TNF-α) expressio...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
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Termedia Publishing House
2016-12-01
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| Series: | Folia Neuropathologica |
| Subjects: | |
| Online Access: | https://www.termedia.pl/Protective-role-of-dexmedetomidine-in-unmethylated-CpG-induced-inflammation-responses-in-BV2-microglia-cells,20,28979,1,1.html |
| Summary: | Unmethylated CpG DNA, as a stimulatory molecule, has potent pro-inflammatory effects in the central nervous system (CNS). Dexmedetomidine (DEX) has been confirmed to exert anti-inflammatory effects in CNS. Our study was aimed to explore the effects of DEX on tumor necrosis factor-α (TNF-α) expression in unmethylated CpG DNA-challenged microglia. In vivo, after 3 d intracisternal injection of ODN1668, we evaluated the severity of meningitis with or without DEX via pathobiology method and detected the expression of TNF-α from molecular and protein levels. In vitro, we explored whether the ODN1668 could activate microglia to express TNF-α and the inhibition mechanism of DEX. Our results demonstrated that DEX could alleviate the severity of ODN1668-induced meningitis. And while BV2 microglia was stimulated by ODN1668 for different time, TNF-α was increased in mRNA and protein levels but the effect was attenuated by DEX via decreasing phosphorylated AKT and ERK |
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| ISSN: | 1641-4640 1509-572X |