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目的:探讨视黄酸(RA)对细胞因子诱导的人肺泡Ⅱ型上皮细胞A549分泌C3及B因子的影响。方法:用ELISA检测TNFα和IL1β诱导的A549细胞培养上清中C3及B因子的水平。用RTPCR分析C3及B因子mRNA的表达。结果:TNFα和IL1β诱导A549细胞分泌C3及B因子具有时间和剂量依赖性。IL6诱导A549细胞分泌C3和B因子的水平是未处理组的4.7、1.4倍,IFNγ诱导A549细胞分泌C3和B因子的水平是未处理组的2.1、1.7倍。RA本身对A549细胞分泌C3及B因子没有影响,但可显著增强TNFα和IL1β诱导的A549细胞分泌C3和B因子及其mRNA的表达,以及IL6和IFNγ诱导的B因子合成。结论:RA可上调TNFα、IL1β、IL6和IFNγ诱导的A549细胞分泌C3及B因子,调节肺局部组织的免疫防御反应,为临床上应用RA和细胞因子防治肺部疾病提供了理论依据。
Objective: To investigate the effects of retinoic acid (RA) on the secretion of C3 and factor B of cytokine-induced human alveolar type II epithelial A549 cells. Methods: The levels of C3 and B in supernatant of A549 cells induced by TNFα and IL1β were detected by ELISA. Analysis of C3 and B factor mRNA expression by RTPCR. Results: TNFα and IL1β induced A549 cells to secrete C3 and factor B in a time-and dose-dependent manner. IL6 induced A549 cells to secrete C3 and B factors at a level of 4.7 and 1.4 times that of untreated cells. IFNγ induced A549 cells to secrete C3 and B at levels 2.1 and 1.7 times that of untreated cells. RA itself had no effect on the secretion of C3 and factor B in A549 cells, but significantly increased the secretion of C3 and factor B and its mRNA by A549 cells induced by TNFα and IL1β, as well as the induction of factor B synthesis by IL6 and IFNγ. CONCLUSION: RA can up-regulate the secretion of C3 and factor B of lung cancer A549 cells induced by TNFα, IL1β, IL6 and IFNγ and regulate the immune defense response in local tissues of lung. It provides a theoretical basis for clinical application of RA and cytokines in the prevention and treatment of pulmonary diseases.