The antioxidant caffeic acid phenethyl ester induces apoptosis associated with selective scavenging of hydrogen peroxide in human leukemic HL-60 cells
The antioxidant caffeic acid phenethyl ester induces apoptosis associated with selective scavenging of hydrogen peroxide in human leukemic HL-60 cells
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DOI：
10.1097/00001813-200102000-00008
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发表时间：
2001-02-01
影响因子：
2.3
通讯作者：
Wang, SY
中科院分区：
文献类型：
--
作者：
Chen, YJ;Shiao, MS;Wang, SY
咖啡酸苯乙酯（CAPE）是蜂胶的一种活性成分，具有抗氧化和肿瘤细胞毒性等多种生物学和药理活性。为了阐明咖啡诱导的氧化还原状态改变与细胞凋亡之间的关系，我们检测了咖啡处理后人类白血病HL-60细胞的细胞死亡类型。6杯/毫升的CAFE处理在第2天显著抑制了70.3 +/- 4.0%的生长。这种抑制作用被n -乙酰- l-半胱氨酸（NAC）预处理部分阻断，琼脂糖凝胶电泳显示，CAFE处理后DNA明显断裂。6小时后，CAFE导致线粒体跨膜电位显著下降至未处理水平的一半左右，1小时后细胞内谷胱甘肽（GSH）迅速耗竭至41.7 +/- 6.0%。NAC预处理HL-60细胞逆转了GSH耗竭，部分挽救了cape诱导的细胞凋亡。在细胞内活性氧方面，CAFE能快速而深刻地清除H2O2（处理2小时后占未处理细胞的19%），但不能清除超氧阴离子。这些结果表明，在人白血病HL-60细胞中，CAFE诱导的细胞凋亡与线粒体功能障碍、GSH消耗和H2O2选择性清除有关。[C] 2001 Lippincott Williams & Wilkins.]
Caffeic acid phenethyl ester (CAPE), an active component of propolis, has many biological and pharmacological activities including antioxidation and tumor cell cytotoxicity. We examined the type of cell death in human leukemic HL-60 cells after CAFE treatment in order to elucidate the relationship between CAFE-induced alterations of the redox state and apoptosis. CAFE treatment (6 mug/ml) resulted in marked growth inhibition up to 70.3 +/- 4.0% at day 2. This inhibition was partially blocked by pretreatment with N-acetyl-L-cycteine (NAC), Agarose gel electrophoresis showed evident DNA fragmentation after CAFE treatment. CAFE induced a significant decrease in mitochondrial transmembrane potential to about halt of the untreated level after 6 h and a rapid depletion of intracellular glutathione (GSH) down to 41.7 +/- 6.0% after 1 h. Pretreatment of HL-60 cells with NAC reversed the GSH depletion and partially rescued cells from CAPE-induced apoptosis. With regard to intracellular reactive oxygen species, CAFE caused a fast and profound scavenging of H2O2 (19% of untreated cells after a 2-h treatment) but not of superoxide anion. These results suggest that apoptosis induced by CAFE is associated with mitochondrial dysfunction, GSH depletion and selective scavenging of H2O2 in human leukemic HL-60 cells. [(C) 2001 Lippincott Williams & Wilkins.].