| 施志超.黄芪甲苷对肾癌细胞系（769-P）增殖、凋亡的影响[J].浙江中西医结合杂志,2022,32(10): |
| 黄芪甲苷对肾癌细胞系（769-P）增殖、凋亡的影响 |
| Effects of astragaloside IV on proliferation and apoptosis of renal cell carcinoma cell line (769-P) |
| 投稿时间：2022-01-21 修订日期：2022-09-09 |
| DOI： |
| 中文关键词: 凋亡 黄芪甲苷 肿瘤 |
| 英文关键词:apoptosis Astragaloside IV cancer |
| 基金项目:浙江省丽水市科技局项目(2020SJZC039) |
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| 摘要点击次数: 629 |
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| 中文摘要: |
| 目的 探讨黄芪甲苷作抗癌症的药理作用及其机制。方法 使用CCK-8法检测黄芪甲苷对肾癌细胞的细胞毒性作用。使用0, 5, 10和20μM浓度黄芪甲苷溶液作用肾癌细胞（769-P）作用24h或48h后，使用ROS探针（DCFH-DA）检测活性氧的变化，使用Annexin V FITC/PI双染法检测细胞凋亡比例变化，使用线粒体膜电位探针（JC-1）检测线粒体膜电位的变化，用分光光度法检测检测活性Caspase 3和Caspase 9的变化水平。结果 5、10、20、40和80μM黄芪甲苷干预 48h 后，769-P细胞活性较对照组显著降低[(85.372±4.60)%、(63.73±3.51)%、 (42.43±5.65)%、(26.57±2.41)%和(18.47±3.23)%比(100.00±0.00)%，P <0.05或0.01]。与对照组比较，黄芪甲苷5、10和20μM处理769-P细胞24h后，ROS荧光强度明显增强[(180274.98±3150.01)、(210165.51±15648.06) 和(264301.56±8331.92)比(153166.22±7782.05)，P<0.05或0.01]，线粒体膜电位JC-1荧光强度比值(FL1-A/FL2-A)明显上升[(2.12±0.07)、(2.61±0.35)和(3.15±0.30)比((1.79±0.16)，P<0.05或0.01]。与对照组比较，黄芪甲苷5、10和20μM处理769-P细胞48h后，凋亡比例明显上升[(51.23±4.66)、(63.01±3.22)和(85.50±3.60)比((1.38±0.65)，P<0.01]，Casapse3活性明显上升[(2.81±0.46)、(3.93±0.72)和(6.08±1.58)比((1.00±0.00)，P<0.01]，Casapse9活性明显上升[(1.44±0.19)、(1.73±0.25)和(2.67±0.12)比((1.00±0.00)，P<0.05或0.01]。结论 黄芪甲苷以浓度依赖性的方式抑制769-P细胞的增殖活性，对769-P细胞有细胞毒性，黄芪甲苷促进了ROS的过度表达，降低了线粒体膜电位，促进Caspase3/9活性的增加，最终诱导细胞凋亡。黄芪甲苷可以对肾癌细胞的毒性与细胞凋亡有关，其可能的机制激活ROS/Caspase通路有关。 |
| 英文摘要: |
| Objective To investigate the pharmacological effect and mechanism of Astragaloside IV on cancer.?Methods The cytotoxicity of Astragaloside IV on renal cell carcinoma cells was detected by CCK-8 test. Use Astragaloside IV solution at concentrations of 0, 5,?10 and 20 μM acted on renal cancer cells (769-P) for 24 or 48 hours, ROS probe (DCFH-DA) was used to detect the changes of reactive oxygen species, Annexin V FITC/PI double staining method was used to detect the changes of apoptosis proportion, mitochondrial membrane potential probe was used.?Results After treatment with 5, 10, 20, 40 and 80 μM Astragaloside IV for 48h, 769-P cell activity compared with the control group significantly reduced [(85.372±4.60) %, (63.73 ±3.51) %, (42.43 ±5.65) %, (26.57 ±2.41) % and (18.47 ± 3.23) % than (100.00 + 0.00) %, P < 0.05 or 0.01). After treatment with Astragaloside IV at 5, 10 and 20μM for 24h, ROS fluorescence intensity increased significantly [(180274.98±3150.01), (210165.51±15648.06) and (264301.56±8331.92) ratio (153166.22±7782.05), P<0.05 or 0.01], mitochondrial membrane potential JC-1 the fluorescence intensity ratio (FL1-A/FL2-A), a significant increase in [(2.12 ± 0.07), (2.61±0.35) and (3.15 ± 0.30) than (1.79 ± 0.16), (P < 0.05 or 0.01). Compared with the control group, the apoptosis rate of 769-P cells treated with Astragaloside IV at 5, 10 and 20μM for 48h increased significantly [(51.23±4.66), (63.01±3.22) and (85.50±3.60) ratio (1.38±0.65), P<0.01]. Casapse3 increased activity of [(2.81± 0.46), (3.93±0.72) and (6.08 + 1.58) than (1.00 ±0.00), (P < 0.01), Casapse9 increased activity of [(1.44 + 0.19), (1.73±0.25) and (2.67 ± 0.12) than ((1.00± 0.00), P <0.05 or 0.01). ?Conclusion Astragaloside IV inhibited the proliferative activity of 769-p cells in a concentration dependent manner, especially cytotoxicity to 769-P cells. Astragaloside IV promoted the overexpression of ROS, reduced the mitochondrial membrane potential, promoted the increase of caspase 3/9 activity, and finally induced apoptosis?Induce apoptosis.The toxicity of Astragaloside IV on renal cell carcinoma cells is related to apoptosis, and its possible mechanism is related to the activation of ROS/Caspase pathway. |
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