Celastrol isolated from Tripterygium regelii induces apoptosis through both caspase-dependent and -independent pathways in human breast cancer cells |
| |
Authors: | Hee-Sun YangJae-Yong Kim Ju-Hye LeeByong-Won Lee Ki-Hun ParkKi-Hwan Shim Mi-Kyung LeeKwon-Il Seo |
| |
Affiliation: | a Department of Food and Nutrition, Sunchon National University, Suncheon 540-742, Republic of Korea b Division of Applied Life Science (BK21 program, IALS), Gyeongsang National University, Jinju 660-701, Republic of Korea |
| |
Abstract: | The aim of the present study was to evaluate the underlying apoptotic mechanisms of celastrol, a major biologically active component of Tripterygium regelii, in human breast adenocarcinoma MCF-7 cells. Celastrol was isolated from T. regelii chloroform extract by silica gel column chromatography, and its chemical structure was identified via 1H NMR and 13C NMR. Celastrol significantly inhibited cell growth in dose- and time-dependent manners. Celastrol induced sub-G1 DNA accumulation, formation of apoptotic bodies, nuclear condensation, and a DNA ladder in MCF-7 cells. Celastrol triggered the activation of caspase family proteins. Celastrol caused activation of caspase-7, -8, and -9, PARP cleavage, caspase-8-mediated bid cleavage, and release of cytochrome c and AIF. In addition, celastrol decreased the expression of anti-apoptotic Bcl-2 protein and increased expression of pro-apoptotic Bax protein. These results suggest that celastrol inhibits the proliferation of MCF-7 cells through induction of apoptosis, which is mediated by a mitochondrial-dependent caspase pathway. |
| |
Keywords: | Tripterygium regelii Celastrol Apoptosis MCF-7 |
本文献已被 ScienceDirect 等数据库收录! |
|