视黄酸对TNF-α和IL-6诱导的肺癌细胞分泌C3和B因子的影响

Effect of retinoic acid on the secretion of C3 and factor B in lung carcinoma cell line A549 induced by TNF-α and IL-6

目的：从免疫治疗的角度探讨近年用来治疗恶性肿瘤的视黄酸（RA）与TNF-α、IL-6相互作用对人肺癌细胞株A549分泌C3及B因子的影响。方法：用ELISA、Western blot的方法检测培养上清中C3及B因子蛋白，用RT-PCR检测细胞内C3及B因子的mRNA。结果：当TNF-α、IL-6和RA分别为10μg／L、50μg／L和1μmol／L时，ELISA、Western blot和RT-PCR法均显示TNF-α、IL-6增进A549细胞分泌C3及B因子和其mRNA表达；RA对A549细胞分泌C3及B因子没有影响；TNF-α组和TNF-α＋RA组培养上清中C3的量分别为91．40±12．59和133．59±11．25（ng／10^6 cells）（P〈0．01），B因子的量分别为100．54±10．39和190．92±15．40（ng／10^6 cells）（P〈0．01）；IL-6组及IL-6＋RA组培养上清中C3的量分别为63．48±9．42和59．89±5．88（ng／10^6 cells）（P〉0．05），B因子的量分别为13．07±2．50和32．89±4．22（ng／10^6 cells）（P〈0．01）；RA（1μmol／L）对B因子的调节作用与TNF-α的浓度有关，随着TNF-α浓度的升高（0～10μL），RA的调节作用减低。结论：RA能上调TNF-α诱导的A549细胞分泌C3和B因子及IL-6诱导的A549分泌B因子。

Objective： To study the effect of retinoic acid （ RA ） which is used in malignant tumor therapy on the secretion of C3 and factor B in human lung cancer cell line A549 induced by TNF-α and IL-6. Methods：C3 and factor B in the culture medium were measured by ELISA and Western blot,the mRNA expression of C3 and factor B was analyzed by RT-PCR. Results：When using TNF-α （ 10μg/L） ,IL-6（50 μg/L） and RA（ 1μmol/L） ,the results of ELISA ,Western blot and RT-PCR showed that TNF-α and IL-6 promoted A549 cells excreting C3 and factor B and their mRNA expression;RA alone did not affect C3 and factor B;in TNF-α group and TNF-α ＋ RA group,the amounts of C3 were 91.40 ±12.59 and 133.59±11.25 （ng/10^6 cells） respectively（P 〈0. 01 ） ,and the amounts of factor B were 100. 54 ± 10. 39 and 190. 92 ± 15.40 （ ng/10^6 cells ） respectively （ P 〈 0. 01 ） ; in IL-6 group and IL-6 ＋ RA group the amounts of C3 were 63.48 ± 9.42 and 59.89 ± 5.88 （ ng/10^6 cells ） respectively （ P 〉 0. 05 ）, and the amounts of factor B were 13.07 ＋ 2. 50 and 32. 89 ± 4.22 （ng/106 cells ） respectively （P 〈 0. 01 ）. The RA （ 1 p.mol/L） regulation to factor B production in A549 cells induced by TNF-α was decreased with the concentration of TNF-α increasing（0 -10 μg/L）. Conclusion：RA may increase secretion of C3 and factor B in A549 cell line induced by TNF-α, and of factor B in A549 cell line induced by IL-6.