摘要
目的:研究红霉素(EM)对烟草烟雾提取物(CSE)作用下人巨噬细胞释放相关炎症因子的影响。方法:体外培养人类单核细胞系U937细胞,在细胞培养液中加入佛波酯(PMA)将其诱导分化为人巨噬细胞。将细胞分为3组:对照组、CSE组、EM+CSE组。CSE组用1%浓度CSE刺激24h,EM+CSE组用1mg/L EM预处理24h后,用1%浓度CSE刺激24h。用液相芯片技术检测各组细胞上清液中嗜酸细胞活化趋化因子(eotaxin)、白介素(IL)-17A、巨噬细胞炎症蛋白(MIP)-1β、单核细胞趋化蛋白(MCP)-1、IL-8、MIP-1α、IL-1β、IL-6含量。结果:CSE显著促进人巨噬细胞释放eotaxin、IL-17A、MIP-1β、MCP-1、IL-8、MIP-1α、IL-1β、IL-6(P<0.05),而EM能抑制CSE引起的上述炎症因子释放增加(P<0.05)。结论:EM可能通过抑制CSE刺激引起的人巨噬细胞释放eotaxin、IL-17A、MIP-1β、MCP-1、IL-8、MIP-1α、IL-1β、IL-6等细胞因子,抑制烟草烟雾暴露相关疾病进展。
Objective:To investigate the effect of erythromycin (EM) on the release of inflammatory cytokines in human macrophages stimulated by cigarette smoke extract (CSE). Methods: The human monocytic cell line U937 cells were cultured in vitro, and differentiated into human macrophages by phorbol esters (PMA). The cells were divided into 3 groups: control group, CSE group (cells were stimulated by 1% CSE), and EM+CSE group (cells were pretreated with 1 mg/L EM for 24 h and then stimulated by 1% CSE). The Luminex LiquiChip was used to measure levels of the following cytokines: eotaxin, interleukin (IL)-17A, macrophage inflammatory protein (MIP)-1β, monocyte chemoattractant protein (MCP)-1, IL- 8, MIP-1, IL-1 and IL-6. Results: CSE significantly promoted the release of inflammatory cytokines (eotaxin, IL-17A, MIP-1β, MCP-1, IL-8, MIP-1α, IL-1β and IL-6) (P 〈0.05), whereas pretreated with EM blocked the effect of CSE ( P 〈0.05). Conclusion: EM could inhibit CSE-induced inflammatory cytokines (eotaxin, IL-17A, MIP-1 β, MCP-1, IL-8, MIP-1α, IL-1β and IL-6) release by human macrophages, which may prevent tobacco smoke exposure related diseases.
出处
《广西医科大学学报》
CAS
2017年第5期663-666,共4页
Journal of Guangxi Medical University
基金
国家自然科学基金资助项目(No.81360012)
广西自然科学基金资助项目(No.2016GXNSFAA380269)
关键词
液相芯片
烟草烟雾提取物
红霉素
炎症因子
liquichip
cigarette smoke extract
erythromycin
inflammatory cytokines