23-hydroxybetulinic acid-induced HL-60 cell autophagic apoptosis and its molecular mechanism

Abstract

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.

Keywords:

• 23-hydroxybetulinic acid
• autophagic
• apoptosis
• HL-60 cell

Acknowledgements

This study was supported by a grant from the Natural Science Foundation of Anhui Province (grant no. 090413123), for which the authors thank them.