| 朱韬,郑有卯.雷公藤红素诱导人骨肉瘤细胞系HOS凋亡及机制研究[J].浙江中西医结合杂志,2015,25(8): |
| 雷公藤红素诱导人骨肉瘤细胞系HOS凋亡及机制研究 |
| Celastrol induces apoptosis in human osteosarcoma cell line HOS. Zhu Tao, Zheng Youmao. Enze Medical Center Luqiao Hospital. Taizhou (318050). China |
| 投稿时间：2015-03-25 修订日期：2015-06-10 |
| DOI： |
| 中文关键词: 雷公藤红素 HOS 凋亡 ROS JNK |
| 英文关键词:celastrol HOS apoptosis ROS JNK |
| 基金项目: |
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| 中文摘要: |
| 目的：探讨雷公藤红素对人骨肉瘤细胞HOS的杀伤作用及其机制。方法：将人骨肉瘤细胞HOS用各种不同的浓度的雷公藤红素治疗后,采用MTT法检测雷公藤红素对HOS细胞活力的抑制作用；采用流式细胞术检测HOS细胞用雷公藤红素处理后细胞的凋亡及ROS的产生；Western blot检测HOS细胞用雷公藤红素处理后cleaved caspase-9、cleaved caspase-3和磷酸化JNK的表达水平。结果：雷公藤红素对HOS细胞活力的抑制效应呈剂量依赖性,1μmol/L雷公藤红素组的细胞活力抑制率为23.6±3.5,2μmol/L 雷公藤红素组细胞活力抑制率为43.7±5.4,3μmol/L 雷公藤红素组细胞活力抑制率为57.8±6.9,4μmol/L 雷公藤红素组细胞活力抑制率为75.5±6.4,5μmol/L 雷公藤红素组细胞活力抑制率为83.7±7.3。雷公藤红素可显著诱导HOS细胞发生凋亡,对照组的凋亡率为2.3±0.5,1μmol/L雷公藤红素组凋亡率为17.2±2.2,3μmol/L 雷公藤红素组凋亡率为39.5±3.6。雷公藤红素可显著诱导HOS细胞ROS的产生,对照组的ROS阳性率为1.3±0.4,1μmol/L雷公藤红素组的ROS阳性率为13.6±1.5, 3μmol/L雷公藤红素组的ROS阳性率为29.4±3.3。雷公藤红素处理后HOS细胞cleaved caspase-9、cleaved caspase-3和磷酸化JNK的表达水平均显著上升。结论：雷公藤红素通过ROS/JNK途径诱导人骨肉瘤细胞发生caspase依赖的凋亡。 |
| 英文摘要: |
| objective: To explore the anti-tumor effect and the mechanism on HOS cells treated with celastrol. Methods: HOS cells were treated with various concentrations of celastrol, and then the cell viability was measured using the MTT assay. Apoptosis induction and ROS production were determined by flow cytometry. The expression of cleaved caspase-9, cleaved caspase-3 and phospho-JNK were evaluated by western blotting. Results: The viability of HOS cells were significantly inhibited by celastrol treatment, and the inhibition rate is as follows: 1μmol/L celastrol group: 23.6±3.5, 2μmol/L celastrol group: 43.7±5.4, 3μmol/L celastrol group: 57.8±6.9, 4μmol/L celastrol group: 75.5±6.4, 5μmol/L celastrol group: 83.7±7.3. Celastrol treatment significantly induced apoptosis in HOS cells, and the apoptotic rate is as follows: control group: 2.3±0.5, 1μmol/L celastrol group: 17.2±2.2, 3μmol/L celastrol group: 39.5±3.6. Celastrol treatment significantly induced ROS production in HOS cells, and the ROS positive rate is as follows: control group: 1.3±0.4, 1μmol/L celastrol group: 13.6±1.5, 3μmol/L celastrol group: 29.4±3.3. Western blotting demonstrated that celastrol significantly up-regulated the expression of cleaved caspase-9, cleaved caspase-3 and phospho-JNK in HOS cells. Conclusion: Celastrol induced caspase dependent apoptotic cell death through ROS/JNK pathway in HOS cells. |
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