| 五味子乙素通过ROS介导内质网应激诱导人乳腺癌MDA-MB-231细胞凋亡的研究 |
| 投稿时间：2021-06-24 修订日期：2021-10-18 点此下载全文 |
| 引用本文：王玮婷,殷雪琴,夏金娥,张夏炎.五味子乙素通过ROS介导内质网应激诱导人乳腺癌MDA-MB-231细胞凋亡的研究[J].药学实践杂志,2021,39(6):499~503,533 |
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| 基金项目:国家自然科学基金（81703882） |
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| 中文摘要:目的 研究五味子乙素对人乳腺癌MDA-MB-231细胞凋亡的影响及其作用机制。方法 用细胞计数试剂(CCK-8)检测不同浓度五味子乙素对MDA-MB-231细胞存活率的影响；五味子乙素（10、20、40 μmol/L）作用 MDA-MB-231 细胞 24 h，分别用Annexin V-FITC/PI检测细胞凋亡情况；用DCFA-DA荧光探针检测细胞内活性氧（ROS）水平；用Western blot法检测细胞凋亡及内质网应激相关蛋白（Bcl-2、Bax、CHOP、GPR78、PERK、p-PERK、p-eIF2α、eIF2）的表达。结果 与空白组比较，随着五味子乙素浓度增大，细胞存活率明显降低，其IC50为19.16 μmol/L；与对照组比较，五味子乙素（10、20、40 μmol/L）均能抑制细胞克隆形成(P<0.05)，且呈剂量依赖；五味子乙素（10、20、40 μmol/L）均可诱导细胞凋亡（P<0.05），使抗凋亡蛋白BCL-2的表达显著降低，促凋亡蛋白Bax的表达显著升高(P<0.05)；五味子乙素（10、20、40 μmol/L）显著升高细胞内ROS水平(P<0.05)，且呈剂量依赖；五味子乙素（10、20、40 μmol/L）能够激发内质网应激，使内质网应激相关蛋白CHOP、GPR78、p-eIF2α表达增多(P<0.05)，且呈剂量依赖。结论 五味子乙素可能通过ROS介导内质网应激诱导MDA-MB-231细胞凋亡。 |
| 中文关键词:五味子乙素 乳腺癌 活性氧 内质网应激 凋亡 |
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| Schisandrin B induces apoptosis of human breast cancer MDA-MB-231 cells through ROS mediated endoplasmic reticulum stress |
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| Abstract:Objective To study the effects of schisandrin B (Sch B) on the apoptosis of human breast cancer MDA-MB-231 cells and its mechanism. Methods Cell counting reagent (CCK-8) was used to detect the effect of Sch B on the survival rate of MDA-MB-231 cells. MDA-MB-231 cells were treated with Sch B (10, 20, 40 μmol/L) for 24 hours. The cell death was detected by Annexin V-FITC/PI. The levels of intracellular reactive oxygen species (ROS) were detected by DCFA-DA fluorescent probe. Apoptosis and the expression of endoplasmic reticulum stress related proteins (Bcl-2、Bax、CHOP、GPR78、PERK、p-PERK、p-eIF2α、eIF2) were detected by Western blot. Results Compared with the blank group, the cell survival rate decreased significantly (P<0.01) with the increase of Sch B concentration, and its IC50 was 19.16 μmol/L. Compared with the control group, Sch B groups (10, 20, 40 μmol/L) inhibited cell clone formation in a dose-dependent manner (P<0.05). Sch B groups (10, 20, 40 μmol/L) induced apoptosis (P<0.05), significantly reduced the expression of anti-apoptotic protein Bcl-2 and significantly increased the expression of pro-apoptotic protein Bax (P<0.05). Sch B groups (10, 20, 40 μmol/L) significantly increased the level of intracellular ROS in a dose-dependent manner (P<0.05). Sch B groups (10, 20, 40 μmol/L) stimulated endoplasmic reticulum stress and increased the expressions of endoplasmic reticulum stress-related proteins CHOP, GPR78 and p-eIF2α in a dose-dependent manner (P<0.05). Conclusion Sch B induces apoptosis of MDA-MB-231 cells through ROS mediated endoplasmic reticulum stress. |
| keywords:schisandrin B breast cancer reactive oxygen species endoplasmic reticulum stress apoptosis |
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