Essential oil of Curcuma wenyujin induces apoptosis in human hepatoma cells
Essential oil of Curcuma wenyujin induces apoptosis in human hepatoma cells作者机构：State Drug Clinical Trial Agency Science & Technology Department Sichuan Provincial People's Hospital Sichuan Academy of Medical Science Chengdu 610072 Sichuan Province China Institute of Chinese Medical Sciences University of Macao Av. Padre Tomas Pereira S.J. Taipa Macao China Institute of Chinese Medicine the Chinese University of Hong Kong Hong Kong China
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2008年第14卷第27期
页 面：4309-4318页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
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
主 题：Essential oil Curcuma wenyujin, Apoptosis HepG2 Caspase-3 Mitochondrial Cytochrome C Cleaved Poly-ADP-ribose polymerase
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.
维普期刊数据库