Nicotine suppresses lipopolysaccharide-induced release of interleukin-6 in mixed glia and microglia-

来源 :Neural Regeneration Research | 被引量 : 0次 | 上传用户:wb_0622
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Inflammation plays an important role in the pathogenesis of Parkinson’s disease (PD) through the over-activation of microglia. Epidemiological studies show that smoking is associated with a lower incidence of PD. This study hypothesized that the neuroprotective effect of nicotine is mediated by modulating the activation of microglia via cytokine release. This study found that nicotine pretreatment suppressed the lipopolysaccharide-induced inflammatory reaction in the nervous system, especially microglia activation and interleukin-6 production. The inhibitory effects of 100 μmol/L nicotine were stronger compared with 1 and 10 μmol/L nicotine. These findings indicate that nicotine significantly decreases the production of proinflammatory interleukin-6 in mixed glia or microglia-enriched cultures, and plays an inhibitory effect on the lipopolysaccharide-induced inflammatory reaction. Inflammation plays an important role in the pathogenesis of Parkinson’s disease (PD) through the over-activation of microglia. Epidemiological studies show that smoking is associated with a lower incidence of PD. This study hypothesized that the neuroprotective effect of nicotine is mediated by modulating the activation of microglia via cytokine release. This study found that nicotine pretreatment suppressed the lipopolysaccharide-induced inflammatory reaction in the nervous system, especially microglia activation and interleukin-6 production. The inhibitory effects of 100 μmol / L nicotine were stronger than 1 and 10 μmol / L nicotine. These results indicate that nicotine significantly reduces the production of proinflammatory interleukin-6 in mixed glia or microglia-enriched cultures, and plays an inhibitory effect on the lipopolysaccharide-induced inflammatory reaction.
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