【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。更多还原

【Abstract】 Objective To investigate the effects of nicotinic acetylcholine receptor(nAChR) on lipopolysaccharide(LPS)-induced secretions of cytokines in microglial cells(MGCs).MethodsCultured 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 24h.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 pro-inflammatory mediators induced by LPS in MGCs.更多还原