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Essential oil of Curcuma wenyujin induces apoptosis in human hepatoma cells

查看全文 作  者:YU [1,2]Xiao;Feng-Qing [2]Yang;Shao-Ping [2]Li;Guang [2]Hu;Simon Ming-Yuen [2,3]Lee;Yi-Tao [2]Wang 高影响力作者 机构地区:[1]State Drug Clinical Trial Agency, Science & Technology Department, Sichuan Provincial People's Hospital, Sichuan Academy of Medical Science, Chengdu 610072, Sichuan Province, China;[2]Institute of Chinese Medical Sciences, University of Macao, Av. Padre Tomas Pereira S.J., Taipa, Macao, China;[3]Institute of Chinese Medicine, the Chinese University of Hong Kong, Hong Kong, China高影响力机构 出  处:《World Journal of Gastroenterology》索引2008年第14卷第27期,共10页高影响力期刊 基  金:Grants from the Research Committee, Universityof Macao, Macao SAR, No RG054/05-06S and RG058/05-06S;grants from the Science and Technology Development Fund, Macao SAR, No 012/2006/A and 045/2007/A3 摘  要:AIM: To investigate the effects of the essential oil of Curcuma wenyujin (CWO) on growth inhibition and on the induction of apoptosis in human HepG2 cancer cells. METHODS: The cytotoxic effect of drugs on HepG2 cells was measured by 3-(4,5-dimethylthiazol-2- yl)-2,5-diphenyltetra-zolium bromide (MTT) assay. DNA fragmentation was visualized by agarose gel electrophoresis. Cell cycle and mitochondrial transmembrane potential (△Ψm) were determined by flow cytometry (FCM). Cytochrome C immunostaining was evaluated by fluorescence microscopy. Caspase-3 enzymatic activity was assayed by the cleavage of Ac-DEVD-R110. Cleaved PARP and active caspase-3 protein levels were measured by FCM using BD? CBA Human Apoptosis Kit. RESULTS: Treatment with CWO inhibited the growth of HepG2 cells in a dose-dependent manner, and the IC50 of CWO was approximately 70 μg/mL. CWO was found to inhibit the growth of HepG2 cells by inducing a cell cycle arrest at S/G2. DNA fragmentation was evidentlyobserved at 70 μg/mL after 72 h of treatment. During the process, cytosolic HepG2 cytochrome C staining showed a markedly stronger green fluorescence than in control cells in a dose-dependent fashion, and CWO also caused mitochondrial transmembrane depolarization. Furthermore, the results clearly demonstrated that both, activity of caspase-3 enzyme and protein levels of cleaved PARP, significantly increased in a dose- dependent manner after treatment with CWO. CONCLUSION: CWO exhibits an antiproliferative effect in HepG2 cells by inducing apoptosis. This growth inhibition is associated with cell cycle arrest, cytochrome C translocation, caspase 3 activation, Poly- ADP-ribose polymerase (PARP) degradation, and loss of mitochondrial membrane potential. This process involves a mitochondria-caspase dependent apoptosis pathway. As apoptosis is an important anti-cancer therapeutic target, these results suggest a potential of CWO as a chemotherapeutic agent. 关 键 词:肝细胞癌 姜黄 香油精 细胞凋亡 细胞色素C
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