首页> 中文期刊> 《天然产物研究与开发》 >Desmosdumotin-C A环衍生物TEP诱导HL-60细胞凋亡作用机制研究

Desmosdumotin-C A环衍生物TEP诱导HL-60细胞凋亡作用机制研究

         

摘要

This study focused on the effects of TEP,an A ring derivative of desmosdumotin-C,on the human acute leukemia HL-60 cell apoptosis,and the underlying mechanisms.TEP-induced apoptosis and its effect on Fas,FasL,Bax,Bcl-2 expression were measured by flow cytometry,and the morphological changes of the apoptosis cells were further observed by transmission electron microscop.The results showed that 24 h after 40 μg/mL TEP treatment,the typical apoptotic morphological changes were induced in HL-60 cell.Meantime,40 μg/mL TEP significantly increased Fas,FasL,and Bax expression (P < 0.05),and decreased Bcl-2 expression (P < 0.05).All the results suggested that TEP effectively induced apoptosis in HL-60 cells,and the mechanism may be involved in upregulating Fas,FasL,Bax expression,and reducing Bcl-2 expression.%本研究主要探讨毛叶假鹰爪素C(Desmosdumotin C)A环衍生物TEP诱导人急性白血病HL-60细胞凋亡作用及机制.流式细胞技术检测TEP诱导细胞凋亡及其对凋亡细胞中Fas、FasL、Bax、Bcl-2表达率的影响,透射电镜观察凋亡细胞形态学改变.结果显示40μg/mL TEP作用细胞24h后,细胞可呈现典型的凋亡形态学变化;40 μg/mL TEP可明显提高凋亡细胞中Fas、FasL、Bax的表达(P<0.05),并可明显降低抗凋亡细胞Bcl-2的表达(P<0.05).以上实验结果表明毛叶假鹰爪素C(Desmosdumotin C,Des C)A环衍生物TEP可有效地诱导HL-60细胞凋亡,其作用机制可能与上调Fas、FasL、Bax表达以及下调Bcl-2表达有关.

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