人参总皂苷和小檗碱对肺癌PG细胞分泌免疫抑制性细胞因子的影响

Effects of ginsenoside and berberine on secretion of immunosuppressive cytokines in lung carcinoma cell line PG

目的:观察人参总皂苷(ginsenoside,Gs)和小檗碱(berberine,Ber)对肿瘤细胞分泌免疫抑制性细胞因子转化生长因子β1(transforming growth factor-beta1,TGF-β1)和前列腺素E_2(prostaglandin E_2,PGE_2)的影响,探讨Gs和Ber对肿瘤免疫逃逸的作用机制。方法:首先建立人肺癌PG细胞与人T淋巴细胞株Jurkat细胞的共培养体系,随机分为Gs(100μg/ml)组、Ber(10μg/ml)组、空白对照组和Jurkat组。用Gs和Ber作用PG细胞24 h后与Jurkat细胞共培养,24 h后倒置显徽镜下观察Jurkat细胞生长的状态;台盼蓝拒染实验计数共培养6 h和24 h后Jurkat活细胞数;流式细胞仪检测共培养24 h后Jurkat细胞的凋亡率;100、50、25μg/ml的Gs和10、5、2.5μg/ml的Ber分别处理PG细胞,并设空白对照组(PG细胞未经药物处理),酶联免疫吸附测定法和放射免疫法检测PG细胞上清液TGF-β1和PGE_2的含量。结果:Jurkat细胞与Gs和Ber处理过的PG细胞共培养后,其数目较空白对照组明显减少,而凋亡率较空白对照组明显增加;Gs和Ber可以增加PG细胞TGF-β1的分泌,对PGE_2的分泌无影响。结论:Gs和Ber可以增强PG细胞导致的Jurkat细胞生长抑制和凋亡,其机制可能与Gs和Ber增加PG细胞分泌TGF-β1有关。

Objective： To observe the effects of ginsenoside （Gs） and berberine （Ber）, two kinds of active components of traditional Chinese herbal medicine, on transforming growth factor-beta1 （TGF-β1） and prostaglandin E2, （PGE2） in PG cells. Methods： Co-culture system of human lung carcinoma cell line PG and human T lymphocyte cell line Jurkat was established. PG cells were treated with Gs （100 μg/ml） and Ber （10 μg/ml） for twenty-four hours, and then cocultured with Jurkat cells. After 24-hour ooculture, the state of Jurkat cells was observed with inverted microscope. The viable count of Jurkat cells was detected by trypan blue staining after 6-and 24-hour coculture, and the apoptosis of Jurkat cells was evaluated by flow cytometry. PG cells were treated with 100. 50. 25 μ/ml Gs and 10, 5, 2, 5 μg/ml Ber respectively, and the content of TGFq31 and PGE2 in PG cells was detected by enzyme-linked immunosorbent assay （ELISA） and radioimmunoassay （RIA） method. Results： After coculture with PG cells treated with Gs and Ber, the number of Jurkat cells was less than blank control group, and the apoptosis rates of Jurkat cells in Gs-and Ber-treated groups were higher than blank control group. Gs and Ber could promote the secretion of TGF-β1 in PG cells, but could not change the level of PGE2. Conclusion： Gs and Ber can promote the growth which may be related to the up-regulation of Gs nhibition and apoptosis of Jurkat cells induced by PG cells, and Ber on TGF-β1 secretion in PG cells.