Title of article :
Apoptosis of human melanoma cells induced by the novel compounds propolin A and propolin B from Taiwenese propolis
Author/Authors :
Chen، نويسنده , , Chia-Nan and Wu، نويسنده , , Chia-Li and Lin، نويسنده , , Jen-Kun، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2007
Pages :
14
From page :
218
To page :
231
Abstract :
We recently demonstrated that two new prenylflavanones, propolin A and propolin B, isolated and characterized from Taiwanese propolis, induced cytotoxicity effect in human melanoma A2058 cells and shows a strong capability to scavenge free radicals. In this study, propolin A effectively induced a cytotoxic effect on five different cancer cell lines. Similar results were obtained for propolin B. DNA flow cytometric analysis and DNA fragmentation ladder indicated that propolin A and propolin B actively induced apoptosis in A2058 cells. To address the mechanism of the apoptosis effect of propolin A and propolin B, we evaluated the apoptosis-related proteins in A2058 cells. The levels of procaspase-8, Bid, procaspase-3, DFF45, and PARP were decreased in dose- and time course-dependent manners. Furthermore, also found propolin A and propolin B was capable of releasing cytochrome c from mitochondria to cytosol. The findings suggest that propolin A and propolin B may activate a mitochondria-mediated apoptosis pathway. On the other hand, our data show that propolin B inhibitied xanthine oxidase activity more efficiently than propolin A or CAPE. However, CAPE suppressed ROS-induced DNA strand breakage more efficiently than propolin A or propolin B. All these results indicated that propolin A and propolin B may trigger apoptosis of A2058 cells through mitochondria-dependent pathways and also shown that propolin A and propolin B were strong antioxidants.
Keywords :
Propolin A , Taiwanese propolis , apoptosis , Xanthine oxidase , Propolin B , Human melanoma cells
Journal title :
Cancer Letters
Serial Year :
2007
Journal title :
Cancer Letters
Record number :
1826022
Link To Document :
بازگشت