中文摘要：

评估熊胆汁粉末的效果的目的(， BBP ) 在 HepG2 人的 hepatocellular 癌房间的生长和 apoptosis 上，并且调查调停的可能的分子的机制它的反癌症活动。方法 HepG2 房间为 24， 48 和 72 h 与 BBP 的 0.41.0 mg/mL 被对待。HePG2 房间的生存能力被 MTT 试金决定。细胞的形态学经由阶段对比显微镜学被观察。有染色的 Annexin-V/propidium idodide 和 5,5,6,6-tetrachloro-1,1,3,3-tetraethyl-benzimidazol-carbocyanine 碘化物(JC-1 ) 的激活荧光的房间排序分析被执行分别地决定房间 apoptosis 和 mitochondrial 膜潜力的损失。caspase-9 和 -3 的激活被比色的试金评估。结果有为 24， 48，或 72 h 的 BBP 的 0.41 mg/mL 的治疗分别地由 7%60% ， 20%90% 或 25%98% 显著地减少了房间生存能力，与未经治疗的控制房间相比(P < 0.01 ) 。另外， BBP 治疗在 HepG2 房间导致了词法变化。而且，在与 BBP 的 0， 0.4， 0.6， 0.8 和 1.0 mg/mL 对待以后， apoptosis 房间(包括早、迟了的 apoptotic 房间) 是 18.0% 琠敨琠楲污 ? 潔慴? 敭湡挠獯 ? 慷 ??? 钸 ? 袕 ?趬 s

英文摘要：

Objective： To evaluate the effect of Bear Bile Powder （熊胆粉, BBP） on the growth and apoptosis of HepG2 human hepatocellular carcinoma cells, and investigate the possible molecular mechanisms mediating its anti-cancer activity. Methods： HepG2 cells were treated with 0.4-1.0 mg/mL of BBP for 24, 48 and 72 h. The viability of HePG2 cells was determined by MTT assay. Cellular morphology was observed via phase-contrast microscopy. Fluorescence-activated cell sorting analysis with Annexin-V/propidium idodide and 5,5＇,6,6＇-tetrachloro- 1 ,1＇,3,3＇-tetraethyl-benzimidazol-carbocyanine iodide （JC-1） staining was performed to determine cell apoptosis and the loss of mitochondrial membrane potential, respectively. Activation of caspase-9 and -3 was evaluated by a colorimetric assay. Results： The treatment with 0.4-1 mg/mL of BBP for 24, 48, or 72 h respectively reduced cell viability significantly by 7%-60%, 20%-90% or 25%-98%, compared with the untreated control cells （P〈0.01）. In addition, BBP treatment induced morphological changes in HepG2 cells. Furthermore, after treated with 0, 0.4, 0.6, 0.8 and 1.0 mg/mL of BBP, apoptosis cells （including early and late apoptotic cells） were 18.0% ± 1.3%, 34.9% ± 2.2%, 33.9% ± 2.8%, 37.4% ± 2.8% and 46.0% ± 2.5%, respectively （P〈0.05）; and the percentage of cells with reduced JC-1 red fluorescence were 6.6% ± 0.8%, 8.5% ± 0.8%, 13.5% ± 1.6%, 17.6%± 2.3% and 46.7% ± 3.6%, respectively （P〈0.01）. Finally, BBP treatment significantly and dose-dependently induced activation of both caspase-9 and caspase-3 in HepG2 cells （P〈0.05）. Conclusions： BBP could inhibit the growth of HepG2 hepatocellular cancer cells through mitochondrion-mediated apoptosis, which may, in part, explain its anti-cancer activity. BBP may be a potential novel therapeutic agent for the treatment of hepatocellular carcinoma.