Effect of Jolkinolide B on apoptosis of adriamycin-resistant leukemia cell lines HL-60/ADR and its mechanism

Objective To explore the role of Fas / Fas L pathway in the apoptosis of adriamycin-resistant leukemia cell lines HL-60 / ADR induced by Jolkinolide B. Methods The apoptosis of HL-60 / ADR cell was detected by Annexin V fulorescein isothiocyanate / propidiumiodide( FITC / PI) staining. The expressions of Fas / Fas L were detected by Western blot. The activity of caspase-8 and caspase-3 was detected by fluorometry. Results The HL-60 / ADR apoptosis rate increased with the increase of concentration of Jolkinolide B and extension of action time of Jolkinolide B. The early apoptosis rates and total apoptosis rates induced by 40 mg·L- 1Jolkinolide B were significantly higher at 24,48 and 72 h than those at 0 h( P 0. 05,P 0. 001). The early apoptosis rates and total apoptosis rates induced by 20,40 and 80 mg·L- 1Jolkinolide B were significantly higher than those of 0 mg·L- 1at 48 h( P 0. 05,P 0. 001). The expression of Fas / Fas L protein and activities of caspase-3and caspase-8 increased with the extension of action time of Jolkinolide B. The activities of caspase-3 and caspase-8 were significantly higher at 24,48 and 72 h than those at 0 h( P 0. 05,P 0. 001). Conclusion Jolkinolide B can induce the apoptosis of adriamycin-resistant leukemia cell lines HL-60 / ADR. Fas / Fas L way participates in the apoptosis of HL-60 / ADR cells induced by Jolkinolide B.