| 史杰.川楝素上调肝癌细胞死亡受体5的表达提高TRAIL的抗肿瘤活性[J].浙江中西医结合杂志,2017,27(11): |
| 川楝素上调肝癌细胞死亡受体5的表达提高TRAIL的抗肿瘤活性 |
| Toosendanin enhances the anti-tumor effect of TRAIL by upregulating the expression of DR5 in hepatocellular carcinoma |
| 投稿时间：2017-03-05 修订日期：2017-05-26 |
| DOI： |
| 中文关键词: 川楝素 DR5 TRAIL 肝细胞肝癌 |
| 英文关键词:toosendanin DR5 TRAIL hepatocellular carcinoma |
| 基金项目: |
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| 中文摘要: |
| 目的: 探讨天然药物活性成分川楝素对TRAIL抗肝癌活性的影响并研究其机制。方法：将HepG2人肝癌细胞按对照组,川楝素组,TRAIL组,川楝素+TRAIL组及川楝素+TRAIL+DR5 siRNA组进行分组,CCK-8法检测HepG2的细胞活力,流式细胞术检测HepG2细胞的凋亡和线粒体膜电位,Western blot实验和流式细胞术检测HepG2细胞表面DR5的表达水平及caspase-8、caspase-3的活化水平。结果：TRAIL+川楝素组HepG2的相对细胞活力(0.42±0.04)显著低于TRAIL单治疗组(0.84±0.07, P<0.05)和川楝素+TRAIL+DR5 siRNA组(0.76±0.06, P<0.05)。TRAIL+川楝素组HepG2的细胞凋亡率(32.7±2.4)显著高于TRAIL单治疗组(9.3±0.9, P<0.05)和川楝素+TRAIL+DR5 siRNA组(13.8±1.1, P<0.05)。川楝素处理对HepG2细胞Bcl-2家族蛋白的表达无明显影响但能显著提高HepG2细胞表面DR5的表达水平。TRAIL+川楝素组HepG2细胞的相对线粒体膜电位(0.26±0.02)显著低于TRAIL单治疗组(0.78±0.06, P<0.05)和川楝素+TRAIL+DR5 siRNA组(0.68±0.05, P<0.05)。TRAIL+川楝素组HepG2细胞的cleaved caspase-8表达水平(0.37±0.04)及cleaved caspase-3表达水平(0.42±0.04)均显著高于TRAIL单治疗组cleaved caspase-8表达水平(0.11±0.04, P<0.05)及cleaved caspase-3表达水平(0.13±0.02, P<0.05)和川楝素+TRAIL+DR5 siRNA组cleaved caspase-8表达水平(0.14±0.02, P<0.05)及cleaved caspase-3表达水平(0.17±0.02, P<0.05)。结论：川楝素上调肝癌细胞死亡受体5的表达提高TRAIL的抗肿瘤活性。 |
| 英文摘要: |
| AIM: To investigate the effect and mechanism of toosendanin on enhancing the anti-tumor effect of TRAIL on hepatocellular carcinoma. Methods: HepG2 cells were divided into control group, toosendanin group, TRAIL group, toosendanin + TRAIL group and toosendanin + TRAIL + DR5 siRNA group. CCK-8 assays were performed to evaluate the viability of HepG2 cells. Flow cytometry analysis was performed to detect the cell apoptosis and mitochondrial membrane potential in HepG2. Western blot and flow cytometry analysis was performed to evaluate the expression of DR5 on HepG2 cell surface and the activation of caspase-8 and caspase-3. Results: Relative cell viability of HepG2 in TRAIL + toosendanin group (0.42±0.04) was significantly lower than the TRAIL group (0.84±0.07, P<0.05) and TRAIL + toosendanin + DR5 siRNA group (0.76±0.06, P<0.05). Apoptotic rate of HepG2 cells in TRAIL + toosendanin group (32.7±2.4) was significantly higher than that in the TRAIL group (9.3±0.9, P<0.05) and TRAIL + toosendanin + DR5 siRNA group (13.8±1.1, P<0.05). Treatment with toosendanin didn’t change the expression of Bcl-2 family proteins but significantly increased the expression of DR5 on the surface of HepG2. Relative mitochondrial membrane potential of HepG2 in TRAIL + toosendanin group (0.26±0.02) was significantly lower than the TRAIL group (0.78±0.06, P<0.05) and TRAIL + toosendanin + DR5 siRNA group (0.68±0.05, P<0.05). Relative expression of cleaved caspase-8 (0.37±0.04) and cleaved caspase-3 (0.42±0.04) in TRAIL + toosendanin group were both higher than the cleaved caspase-8 (0.11±0.04) and cleaved caspase-3 (0.13±0.02) in TRAIL group and the cleaved caspase-8 (0.15±0.02) and cleaved caspase-3 (0.17±0.02) in TRAIL + toosendanin + DR5 siRNA group. Conclusion: Toosendanin enhances the anti-tumor effect of TRAIL by upregulating the expression of DR5 in hepatocellular carcinoma. |
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