【摘要】 目的:观察尼古丁对脂多糖(LPS)诱导的原代大鼠脑皮层小胶质细胞激活的影响及对细胞因子白细胞介素6(IL-6)表达的影响,探讨尼古丁在PD中的可能作用机制。方法:培养原代大鼠脑皮质胶质细胞,纯化小胶质细胞,用尼古丁预处理30min,再加入LPS,采用ELISA检测小胶质细胞不同时间点分泌IL-6的水平及免疫细胞化学检测小胶质细胞特异的离子钙结合蛋白(Iba1)的阳性细胞数。结果:激活的小胶质细胞胞体增大,活化标记物Iba1表达上调;ELISA方法测定显示10μg/LLPS致小胶质细胞在4、8和24h分泌细胞因子IL-6的量与对照组比较均增加(t=14.115、23.530和32.076,P均<0.05),其中在4和8h分泌IL-6的量差异无统计学意义,达到高峰;但经尼古丁(100μmol/L)预处理后,尼古丁和LPS有交互作用,小胶质细胞的激活被抑制(F交互=13.418,P=0.006),且在4h分泌IL-6的量减少(F交互=92.569,P<0.001)。结论:尼古丁可能对LPS引起的炎症反应具有保护作用。更多还原

【Abstract】 Aim:To observe the effects of nicotine on LPS-induced primary rat cortical microglia activation and cytokine IL-6 expression and to explore the possible mechanism of nicotine in PD.Methods:Primary rat cortical glial cells were cultured and microglial cells were purified,with or without nicotine and/or LPS.The IL-6 secretion concentration of microglia at different time was detected by ELISA and the activation of microglia(Iba1 positive cells) was detected by immunocytochemical staining.Results:LPS induced activation of microglia,activated microglia increased the expression of activation marker Iba1.10 μg/L LPS induced the amount of cytokine IL-6 secretion of microglia at 4,8 and 24 h respectively were significantly higher than those of the control group(t=14.115,23.530,and 32.076,P<0.05).The secretion of IL-6 had no significant difference between the amount at 4 and 8 h in microglia,which reached a peak;but pretreatment of cells with nicotine significantly inhibited microglia activation(F=13.418,P=0.006) and the LPS-induced IL-6 production(F=92.569,P<0.001).Conclusion:Nicotine may has protective effect against LPS-induced inflammatory response.更多还原