中文摘要：

瞄准：为了调查反肿瘤，在 vitro 并且在 vivo，和它的机制在 hepatocellular 癌(HCC ) 上人参皂甙 Rg3 工作。方法：Hep1-6 和 HepG2 房间被 Rg3 在 vitro 在不同集中(0， 50， 100 和 200 g/mL ) 对待。在为 0， 6， 12， 24 和 48 h 的孵化以后，房间生存能力被 3- 测量(4， 5-dimethylthiazol-2-yl )-2, 5-diphenyltetrazolium 溴化物试金。Apoptosis 被终端 deoxynucleotidyl 识别标记的调停 transferase 的 dUTP-biotin 刻痕结束。Caspase-3 活动被色基 p-nitroanilide 和流动 cytometry 测量。Bcl-2 家庭蛋白质被查明由西方弄污。线粒体膜潜力被 5 检测， 5， 6 6 - tetrachloro-1， 1， 3， 3 - tetraethylbenzimidazolylcarbocyanine 碘化物。四十个肝忍受肿瘤的 C57Bl6 老鼠为 intra 肿瘤注射随机被划分成 4 个组盐，人参皂甙 Rg3， cyclophosphamide (CTX ) 和人参皂甙 Rg3 + CTX 联合。结果：幸存时间被跟随直到 102 d。在在控制与那些相比给重要增加的幸存时间看的 Rg3 + CTX 组的老鼠组织(P < 0.05 ) 。Rg3 能禁止 HCC 房间增长并且在集中和时间依赖者举止在 vitro 导致房间 apoptosis。减少也导致了线粒体膜潜力。Caspase-3 激活能被禁止者 z-DEVD-FMK 堵住。当 Bcl-2 和 Bcl-XL 在 Rg3 处理以后是下面调整的时， Bax 是起来调整的。结论：我们的数据建议与 CTX 独自一个或联合的 Rg3 在 vivo 禁止了肿瘤生长并且由由 Bcl-2 家庭蛋白质的表达式改变经由内在的小径导致 HCC 房间 apoptosis 延长了鼠标幸存时间。

英文摘要：

AIM：To investigate the anti-tumor function of ginsenoside Rg3 on hepatocellular carcinoma（HCC） in vitro and in vivo,and its mechanism.METHODS：Hep1-6 and HepG2 cells were treated by Rg3 in different concentrations（0,50,100 and 200 μg/mL） in vitro.After incubation for 0,6,12,24 and 48 h,cell viability was measured by 3-（4,5-dimethylthiazol-2yl）-2,5-diphenyltetrazolium bromide assay.Apoptosis was identified by terminal deoxynucleotidyl transferasemediated dUTP-biotin nick end labeling.Caspase-3 activity was measured by chromophore p-nitroanilide and flow cytometry.Bcl-2 family proteins were ascertained by Western-blotting.Mitochondria membrane potentialwas detected by 5,5＇,6＇ 6＇-tetrachloro-1,1＇,3,3＇-tetraethylbenzimidazolylcarbocyanine iodide.Forty liver tumor-bearing C57Bl6 mice were divided randomly into 4 groups for intra-tumor injection of saline,ginsenoside Rg3,cyclophosphamide（CTX） and ginsenoside Rg3 ＋ CTX combination.RESULTS：The survival time was followed up to 102 d.The mice in the Rg3 ＋ CTX group showed significant increased survival time compared with those in the control group（P 0.05）.Rg3 could inhibit HCC cell proliferation and induce cell apoptosis in vitro in the concentration and time dependent manner.It also induced mitochondria membrane potential to decrease.Caspase-3 activation can be blocked by the inhibitor z-DEVD-FMK.Bax was up-regulated while Bcl-2 and Bcl-XL were down-regulated after Rg3 treatment.CONCLUSION：Our data suggested that Rg3 alone or combined with CTX inhibited tumor growth in vivo and prolonged mouse survival time by inducing HCC cell apoptosis via intrinsic pathway by expression alterations of Bcl-2 family proteins.