摘要
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 pmol/L nicotine were stronger compared with 1 and 10 iJmol/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 pmol/L nicotine were stronger compared with 1 and 10 iJmol/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.
基金
Supported by the National Natural Science Foundation of China, No. 30671103
