目的探讨香烟烟雾(Cigarette smoke extract,CSE)对清道夫受体A(scavenger receptor,SR-A)介导炎症相关性研究。方法制备CSE,5%、10%和15%浓度CSE刺激小鼠肺泡巨噬细胞(MH—S)6、12和24小时后,用实时荧光定量聚合酶链反应(PCR)技术检测SR-A表达水平,酶联免疫吸附测定(ELISA)法测定炎症因子IL-6、肿瘤坏死因子α(TNF-α)表达水平。结果CSE刺激巨噬细胞6小时、12小时和24小时后,与空白对照组相比,SR—A表达水平升高,SR—A表达水平随着研究的时间延长而逐渐升高(P〈0.01)。而相对应时间IL-6和TNF-α表达水平分别与空白对照相比,都显著升高且差异有统计学意义(P〈0.01)。通过直线相关分析统计得出SR—A表达水平与IL-6表达水平呈正相关(P〈0.05),与TNF-α表达水平亦呈正相关(P〈0.01)。结论香烟烟雾刺激肺泡巨噬细胞后SR—A表达水平升高,且SR-A表达与炎症因子IL-6、TNF-α表达成正相关,SR—A可能参与介导CSE诱导的肺泡巨噬细胞的炎症反应。
Objective Correlation between inflammation mediated by cigarette smoke extract (CSE) on the scavenger receptor was detected. Methods CSE was prepared and mouse alveolar macrophage (MH-S) was stimulated by different concentration of CSE ( 5%, 10 %, 15%) and different time (6,12,24 hours), Real-time polymerase chain reaction detected the SR-A expression levels, enzyme- linked immunosorbent assay (ELISA) measured the level of IL-6 and TNF-α. Results CSE stimulated MH-S for 6 hours,12 hours and 24 hours,the expression level of SR-A was higher than that in control group and increased steadily with extending time (P 〈 0.01 ). IL-6 and TNF-α expression levels, compared with the control, were significantly increased ( P 〈 0.01). The expression level of SR-A was positively correlated with concentration of IL-6 and TNF-α by linear correlation analysis ( P 〈 0.05). Conclusions There is an up-regulated expression of SR-A by CSE-stimulated mouse alveolar macrophage, and SR-A expression level is positively correlated with levels of IL-6 and TNF-α. SR-A might involved in mediating the alveolar maerophage inflammatory response induced by CSE.