[摘要] 目的：探讨人参皂苷Rg3 联用肿瘤坏死因子相关凋亡诱导配体（TRAIL）对肺癌H358 细胞凋亡的影响及其作用机制。方法:肺癌H358 细胞培养完成后，0、50、100、200 ng/ml TRAIL 或0、25、50、100 μmol/L Rg3 作用H358 细胞48 h，按照实验方法分为对照组、50 μmol/L Rg3 组、100 ng/ml TRAIL 组及50 μmol/L Rg3+100 ng/ml TRAIL 组。MTT法检测Rg3 和/或TRAIL 对肺癌H358 细胞增殖的影响，DAPI 染色荧光倒置显微镜观察Rg3 和/或TRAIL 对肺癌H358 细胞形态学变化的影响，流式细胞术检测Rg3 和/或TRAIL 对肺癌H358 细胞凋亡的影响,WB实验检测Rg3 和/或TRAIL 对各组肺癌H358 细胞内死亡受体（DR5）及caspase-8 表达的影响。结果：50 μmol/L Rg3+100 ng/ml TRAIL 组与其他各组比较，肺癌H358 细胞的增殖抑制最明显（P<0.05）；DAPI染色后显示，50 μmol/L Rg3+100 ng/ml TRAIL组多数胞核皱缩，染色质凝集，荧光强度增加，并出现饱和碎裂等晚期凋亡形态学改变；50 μmol/L Rg3+100 ng/ml TRAIL组与其他各组比较，细胞凋亡率升高最明显，细胞内DR5 及caspase-8 表达增强最明显（均P<0.05）。结论：人参皂苷Rg3 联合TRAIL能够协同抑制肺癌H358 细胞的增殖及诱导细胞凋亡，其作用机制可能与人参皂苷Rg3 协同促进DR5 及caspase-8 的表达上调有关。

[Abstract] Objective: To investigate the effect of ginsenoside Rg3 combined with TRAIL on the apoptosis of lung cancer H358 cells and its possible mechanism. Methods: After the completion of cell culture, H538 cells were treated with TRAIL (0, 50, 100, 200 ng/ml ) or Rg3 (0, 25, 50, 100 μmol/L) for 48 h, and the cells were grouped according to different treatments, namely control group, 50 μmol/L Rg3 group, 100 ng/ml TRAIL group and 50 μmol/L Rg3+100 ng/ml TRAIL group. The effects of Rg3 and/or TRAIL on the proliferation of H358 cells were detected by MTT assay. The effects of Rg3 and/or TRAIL on the morphological changes of H358 cells were observed by DAPI staining. Theapoptosis of H358 cells in each group was detected by flow cytometry. The effects of Rg3 and/or TRAIL on the expressions of death receptor 5 (DR5) and caspase-8 in H358 cells were detected by WB. Results: Compared with the other groups, the proliferation of lung cancer H358 cells was significantly inhibited, while the apoptosis was significantly elevated in the 50 μmol/L Rg3+100 ng/ml TRAIL group (P<0.05). After color developing, cells in 50 μmol/L Rg3+100 ng/ml TRAIL group had nuclear shrinkage, chromatin condensation, increased fluorescence intensity, and late morphological changes such as saturation fragmentation.Compared with the other groups, the expression levels of DR5 and caspase-3 ,8 in the cells of 50 μmol/L Rg3+100 ng/ml TRAIL group were significantly increased (P<0.05). Conclusion: Ginsenoside Rg3 combined with TRAIL can synergistically inhibit the proliferation and induce apoptosis of lung cancer H358 cells. The mechanism may be related to the up-regulation of DR5 and caspase-8 by ginsenoside Rg3.