Department of Oncology, Wannan Medical College, Wuhu 241001, China.
Nat Prod Res. 2012;26(11):1063-8. doi: 10.1080/14786419.2011.559639. Epub 2011 Oct 18.
This study investigates the effects of 23-hydroxybetulinic acid (23-HBA) in inducing HL-60 autophagic apoptosis and explores its potential molecular mechanism. The generation depression effects of HL-60 cells cultured in vitro were detected using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method (p < 0.05), and dosage time-dependent relationships were found. Numerous autophagic vacuoles and empty vacuoles were observed in HL-60 cells treated with 12.5 µM 23-HBA for 24 h by electron microscopy; it was also observed that the process of cell division diminished. Using flow cytometry, the number of apoptotic cells was seen to obviously increase, and the G1/S phase was retarded. It was observed that 23-HBA tended to arrest cells at the G1 phase of the cell cycle. The percentage of the apoptotic cells increased as treatment duration and concentration increased. Beclin-1 expression enhanced with an increase in 23-HBA concentration. We can conclude that 23-HBA can induce autophagic apoptosis in HL-60; the autophagic apoptosis induced by 23-HBA is related to the upregulation of expression of the apoptotic gene beclin-1.
本研究探讨了 23-羟基白桦酸（23-HBA）诱导 HL-60 自噬凋亡的作用，并探讨了其潜在的分子机制。采用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐法（p<0.05）检测体外培养 HL-60 细胞的生成抑制作用，并发现了剂量-时间依赖性关系。电镜下观察到 12.5µM 23-HBA 处理 24h 的 HL-60 细胞中出现大量自噬空泡和空泡；还观察到细胞分裂过程减少。通过流式细胞术，观察到凋亡细胞数量明显增加，G1/S 期被延迟。观察到 23-HBA 倾向于使细胞停滞在细胞周期的 G1 期。随着处理时间和浓度的增加，凋亡细胞的百分比增加。Beclin-1 表达随 23-HBA 浓度的增加而增强。我们可以得出结论，23-HBA 可以诱导 HL-60 发生自噬凋亡；23-HBA 诱导的自噬凋亡与凋亡基因 beclin-1 表达的上调有关。
