| 肖 嘎,杨 锐,吴 涛,党 玲,宋 涛,董昌利.补骨脂酚通过激活ROS强化TRAIL的抗肝细胞癌HepG2细胞作用的机制研究[J].现代生物医学进展英文版,2018,(20):3835-3839. |
| 补骨脂酚通过激活ROS强化TRAIL的抗肝细胞癌HepG2细胞作用的机制研究 |
| Bakuchiol Enhanced TRAIL Induced HepG2 Cell Apoptosis through Activating Oxidative Stress |
| Received:February 28, 2018 Revised:March 28, 2018 |
| DOI：10.13241/j.cnki.pmb.2018.20.007 |
| 中文关键词: 肝细胞肝癌 补骨脂酚 肿瘤坏死因子相关凋亡诱导配体 氧化应激 死亡受体 |
| 英文关键词: Hepatocellular carcinoma Bakuchiol Tumor necrosis factor- related apoptosis-inducing ligand Oxidative stress Death receptors |
| 基金项目:陕西省科学技术研究发展计划项目（2013K12-03-06） |
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| 中文摘要: |
| 摘要 目的：探究补骨脂酚（Bakuchiol，Bak）对肿瘤坏死因子相关凋亡诱导配体（Tumor necrosis factor- related apoptosis-inducing ligand，TRAIL）抗HepG2细胞作用的影响及内在机制。方法：常规培养HepG2细胞，给予梯度浓度的Bak处理，检测细胞活力。联合应用Bak与TRAIL处理，检测细胞活力。Western blot检测Bak处理后氧化应激水平、死亡受体4（Death Receptor 4，DR4）、DR5的表达变化。联合应用Bak与TRAIL检测凋亡情况。进而引入ROS清除剂NAC，联合NAC处理后，检测ROS、DR4、DR5以及凋亡情况。结果：Bak剂量依赖地抑制了HepG2细胞的活力，联合应用Bak+TRAIL对细胞活力的抑制作用优于单独用药。Bak处理后氧化应激水平升高，体现在ROS增加，GSH水平下降；Western blot检测发现Bak处理后DR4、DR5表达增加。联合应用Bak+TRAIL显著增加了细胞凋亡蛋白Bax的表达，抑制了抗凋亡蛋白Bcl2的表达。引入ROS阻断剂NAC处理后，与Bak+TRAIL组相比，ROS水平下降，DR4、DR5表达减少。凋亡检测发现NAC处理降低了Bak+TRAIL引起的细胞凋亡。结论：Bak可以显著增强TRAIL引起的HepG2细胞凋亡，该作用可能与Bak激活氧化应激进而上调DR4、DR5表达有关。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the roles of Bakuchiol (Bak) on HepG2 cell and the effects of co-treatment of Bak and Tumor necrosis factor- related apoptosis-inducing ligand (TRAIL) on HepG2 cells, as well as the inner mechanisms. Methods: Cells were treated with different concentrations of Bak or Bak+TRAILand cell vitality was detected 24 h later. After Bak treatment, cell oxidative stress levels were examined through DCF-DA staining and ROS, GSH detection. Western blot analysis was conducted to detected the expressions of Death receptor 4 (DR4) and DR5. After Bak+TRAIL treatment, cell apoptosis status was detected. Furthermore, ROS scavenger NAC was used to inhibit oxidative stress and DR4, DR5, Bax expressions were detected. Results: Both Bak and TRAIL can reduce HepG2 cell vitality. Co-treatment of Bak and TRAIL further reduced the cell vitality. Bak treatment increased ROS production, DR expressions and reduced cellular GSH level. Co-treatment of Bak and TRAIL induced higher level of apoptosis compared with single-drug treatment. Compared with the Bak + TRAIL group, NAC treatment reduced ROS level and reduced DR expression, as well as the Bak+TRAIL induced apoptosis levels. Conclusion: Bak enhances TRIAL induced HepG2 cell apoptosis and tumor growth via activating cellular oxidative stress and up regulating DR4 and DR5 expressions. |
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