细胞自噬对岩大戟内酯B诱导的白血病细胞HL-60凋亡的影响

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Abstract Objective To investigate the effects of apoptosis of the autophagy-specific inhibitor 3-methyladenine (3-MA) and autophagy agonist rapamycin (RAPA) on the human leukemia cell line HL-60 cells induced by Jolkinolide B. Methods The expressions of autophagy-related protein LC3-Ⅱ/LC3-Ⅰand autophagy regulator Beclin-1 induced by different doses of Jolkinolide B at different time points were detected by Western blot method. The HL-60 cells were divided into blank control group, Jolkinolide B group, Jolkinolide B combined with 5 mmol/L 3-MA group, Jolkinolide B combined with 10 mmol/L 3-MA group, Jolkinolide B combined with 10 nmol/L RAPA group and Jolkinolide B combined with 20 nmol/L RAPA group. Apoptosis of human leukemia cell line HL-60 cells was detected by Annexin V-FITC/PI double staining flow cytometry. Moreover, the activity of Caspase-3 was detected. Results Jolkinolide B could induce autophagy in leukemia cell line HL-60, increase the expression of LC3-Ⅱ and autophagy regulator Beclin-1 (P < 0.05). 3-MA could lower the apoptosis rate of HL-60 cells and the activity of Caspase-3 activity induced by Jolkinolide B (P < 0.05), while RAPA increased the apoptosis rate of HL-60 cells and the activity of Caspase-3 induced by Jolkinolide B (P < 0.05). Conclusion Jolkinolide B can induce autophagy in HL-60 cells, and autophagy plays an important role in the apoptosis of HL-60 cells induced by Jolkinolide B.

Key words： Jolkinolide B Leukemia HL-60 cell Apoptosis Autophagy

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	WANG Jiahe WANG Chao

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WANG Jiahe WANG Chao. Effect of cell autophagy on apoptosis of HL-60 cells induced by Jolkinolide B[J]. 中国医药导报, 2018, 15(28): 13-16细胞自噬对岩大戟内酯B诱导的.

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http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2018/V15/I28/13

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