尼古丁受体参与小胶质细胞炎性因子的释放  

Nicotinic acetylcholine receptor is involved in the secretion of cytokines in microglial cell

作　　者：蔡姝[1] 嵇富海[1] 张慧娟[1] 杨建平[1] 

机构地区：[1]苏州大学附属第一医院麻醉科,215006

出　　处：《江苏医药》2010年第3期322-324,共3页Jiangsu Medical Journal

摘　　要：目的研究尼古丁受体(nAChR)对细菌脂多糖(LPS)诱导的小胶质细胞(MGCs)炎性反应的影响。方法体外培养大鼠MGCs,以LPS诱导MGCs的炎性反应。实验随机分为4组:空白对照组(C组)、LPS对照组(L组)、nAChR激动剂尼古丁干预组(N组)、nAChR拮抗剂美加明干预组(M组)。收集细胞培养液,应用ELISA法检测MGCs的炎性介质肿瘤坏死因子α(TNF-α)、白细胞介素-1β(IL-1β)。收集细胞爬片固定后行SP法免疫细胞化学染色观察小胶质细胞表面补体Ⅲ型受体(OX-42)。结果与C组和N组比较,L组TNF-α、IL-1β表达明显增加,OX-42显色明显加深(P<0.05);L组与M组TNF-α、IL-1β表达及OX-42显色均无明显差异(P>0.05)。结论LPS可激活MGCs,使其表达TNF-α、IL-1β增加,OX-42增加;nAChR参与LPS诱导的MGCs的炎性反应,其激动剂尼古丁可抑制MGCs的炎症反应。Objective To investigate the effects of nicotinic acetylcholine receptor（nAChR） on lipopolysaccharide（LPS）-induced secretions of cytokines in microglia] cells（MGCs）. Methods Cultured rat MGCs were divided into 4 groups of blank control（group C） ,LPS（group L） ,nicotine＋LPS（group N） ,mecamylamine＋LPS（group M）. Cell-free supernatants were collected and assayed for TNF-α and IL-1β release by ELISA after the cells were charged for 4 h and 24 h. Cultured MGCs were plated onto sterile glass cover slips, and OX-42 was accessed by immunohistochemistry analysis. Results LPS- induced increases in the expressions of TNF-α, IL-1βand OX-42 were significantly higher in group L than those in groups of C and N （P〈0. 05）. The expressions of TNF-α, IL-1βand OX-42 were not significantly different between groups of L and M （P〉0. 05）. Conclusion LPS can activate MGCs, increase the secretion of TNF-α and IL-1β, and enhance the expression of OX-42. nAChR is involved in the expression of cytokines induced by LPS in MGCs. The nicotine inhibits the expression of proinflammatory mediators induced by LPS in MGCs.

关 键 词：小胶质细胞 尼古丁受体 尼古丁 美加明 

分 类 号：R363[医药卫生—病理学]