摘要
目的 探讨脂多糖(LPS)对气道上皮细胞(BEAS-2B)损伤后炎性细胞因子分泌的调控作用.方法 采用LPS诱导BEAS-2B发生炎性损伤,于刺激后3、6、12和24h收集细胞上清液,ELISA法测定细胞上清液中IL-8、IL-6、IL-17、IL-1β、胸腺基质淋巴细胞生成素(TSLP)、IL-13、IL-33和单核细胞趋化蛋白1(MCP-1)水平,硝酸还原法检测细胞上清液中NO水平.结果 与正常组相比,LPS可促进BEAS-2B细胞中IL-8、IL-6、IL-17和MCP-1分泌,且诱导3、6、12和24h时均能使IL-8、IL-6、IL-17和MCP-1因子水平显著增加,但不同因子分泌达峰时间不一致;此外,LPS对BEAS-2B细胞IL-1β、TSLP、IL-13、IL-33和NO分泌无显著刺激作用.结论 LPS刺激的BEAS-2B细胞损伤模型适用于IL-8、IL-6、IL-17和MCP-1因子调节相关的机制研究.
Abstract
Objective To determine the regulatory effect of lipopolysaccharide(LPS)on the secretion of inflammatory cytokines after epithelial cell(BEAS-2B)injury in the airway.Methods LPS was used to induce inflammatory injury in BEAS-2B.Cell supernatants were collected at 3 h,6 h,12 h and 24 h after the stimulation,and the levels of IL-8,IL-6,IL-17,ILL-1β,TSLP,IL-13,IL-33 and MCP-1 in the cell supernatants were measured by ELISA,and NO levels in cell supernatants were detected via nitrate reduction.Results LPS promoted the secretion of IL-8,IL-6,IL-17 and MCP-1 in BEAS-2B cells,and all the induction time(3,6,12,and 24 h)greatly increased the levels of IL-8,IL-6,IL-17 and MCP-1 factors,but the peak secretion time of different factors was not consistent.In addition,LPS did not significantly stimulate the secretion of IL-1β,TSLP,IL-13,IL-33 and NO in BEAS-2B cells.Conclusion The LPS-stimulated BEAS-2B cell injury model is suitable in the mechanism study on the regulation of IL-8,IL-6,IL-17 and MCP-1 factors.
基金项目
陕西省重点研发计划(2021ZDLSF04-06)
陕西省重点研发计划(2022ZDXM-SF-06)
陕西省自然科学基础研究计划(2023-JC-QN-0820)
陕西省"秦药"研发重点实验室(2021-QYPT-001)
秦创园中医药创新研发转化项目(2022-QCYZH-006)
陕西省中医医院苗圃培优计划(2021-13)
维普
万方数据