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首页> 外文期刊>Cellular Physiology and Biochemistry >Saikosaponin-D Enhances Radiosensitivity of Hepatoma Cells under Hypoxic Conditions by Inhibiting Hypoxia-Inducible Factor-1α
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Saikosaponin-D Enhances Radiosensitivity of Hepatoma Cells under Hypoxic Conditions by Inhibiting Hypoxia-Inducible Factor-1α

机译：Saikosaponin-D通过抑制缺氧诱导因子-1α增强缺氧条件下肝癌细胞的放射敏感性

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biBackground /i/bOur previous study revealed that the combination of Saikosaponin-d bi(/i/bSSd) and radiation is more effective in the treatment of liver cancer than the application of either of these monotherapeutic methods. However, the molecular mechanisms of the radiosensitizing effect of SSd on liver cancer remained ill defined. biMethods /i/bCells were treated with different interventions; afterward, cell viability, apoptosis, and cell survival of SMMC-7721 and HepG2 hepatoma cells were examined. Xenograft tumor models were established by subcutaneously injecting SMMC-7721 cells. The molecular mechanism was assessed by western blot. biResults /i/bSSd dose-dependently increased radiosensitivity of hepatoma cells under hypoxic condition. The growth inhibitory effect of the combined treatment was correlated with cell apoptosis. Further mechanistic analysis indicated that SSd induced the upregulation of p53 and Bax as well as the downregulation of Bcl-2 by attenuating HIF-1α expression under hypoxic condition. These effects were enhanced when the HIF-1α inhibitor PX-478 was introduced. iIn vivo/i data also presented a more significant suppression of tumor xenograft growth from the combined therapy than from either of the monotherapeutic methods. biConclusions /i/bOur study provides evidence for a radiosensitizing effect of SSd on hepatoma cells under hypoxic conditions by inhibiting HIF-1α expression. Thus, SSd can be used as a potential sensitizer in hepatoma radiotherapy.
机译：背景 我们之前的研究表明，皂苷-d （ SSd）和放射线的结合在治疗中更有效。肝癌的治疗要比以上任何一种单一治疗方法的应用都重要。然而，SSd对肝癌的放射增敏作用的分子机制仍然不清楚。 方法 对细胞进行了不同的干预;之后，检查SMMC-7721和HepG2肝癌细胞的细胞存活率，凋亡和细胞存活率。通过皮下注射SMMC-7721细胞建立异种移植肿瘤模型。通过蛋白质印迹评估了分子机理。 结果 SSd在低氧条件下剂量依赖性地增加肝癌细胞的放射敏感性。联合治疗的生长抑制作用与细胞凋亡有关。进一步的机理分析表明，在缺氧条件下，SSd通过减弱HIF-1α的表达诱导p53和Bax的上调以及Bcl-2的下调。当引入HIF-1α抑制剂PX-478时，这些作用会增强。 体内数据还显示，与任何一种单一治疗方法相比，联合治疗对肿瘤异种移植物生长的抑制作用更大。 结论 我们的研究为低氧条件下SSd通过抑制HIF-1α的表达对肝癌细胞的放射增敏作用提供了证据。因此，SSd可用作肝癌放疗的潜在敏化剂。

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