摘要
目的探讨尼古丁(NIC)对脂多糖(LPS)诱导小鼠脑小胶质细胞激活的影响。方法将32只小鼠随机分为正常对照(CON)组、NIC组、LPS组、NIC+LPS组,每组各8只。NIC+LPS组首先腹腔注射尼古丁建立慢性暴露尼古丁的动物模型,后腹腔注射脂多糖诱导小鼠脑小胶质细胞激活;LPS组同时间只腹腔注射等量脂多糖;NIC组仅腹腔注射尼古丁;CON组腹腔注射等量生理盐水。免疫组织化学方法检测大脑皮质、海马、黑质CD11b阳性小胶质细胞表达情况。结果CD11b阳性小胶质细胞表达NIC组与CON组无差异,LPS组和NIC+LPS组均高于CON组(P<0.01),并且NIC+LPS组明显低于LPS组(P<0.01)。结论慢性NIC处理可以抑制LPS诱导的小鼠脑小胶质细胞激活,提示尼古丁可能对LPS引起的炎症反应具有保护作用。
Objective To investigate the effect of nicotine on the activity of microglia induced by hpopolysaccharideslps （LPS） in the brain of mice.Methods 32 mice were divided averagely into control, nicotine（NIC）,LPS, NIC＋LPS groups randomly. The positive microglia with CD11b antibody in cerebral cortex,hippocampus and substantia nigra were deteced by immunohistochemistry.Results The positive microglia with CD11b expression in NIC were similar to those in control,higher in LPS and NIC＋LPS groups than in control,much lower in NIC＋LPS groups than in LPS. Conclusion Chronic nicotine exposure can inhibit the activity of microglia induced by LPS in the brain of mice,which suggests that nicotine may have the protective effect on inflammatory reaction by LPS treatment.
出处
《解剖科学进展》
CAS
2007年第4期293-296,共4页
Progress of Anatomical Sciences
