尾-d-Glucosyl-(1-4)-伪-l-thevetosides of 17尾-digitoxigenin from seeds of Cerbera manghas L. induces apoptosis in human hepatocellular carcinoma HepG2 cells

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• 作者：Bo Feng^a ; Yue-Wei Guo^b ; Cai-Guo Huang^a ; ^{jiaobh@uninet.com.cn} ; Liang Li^b ; Bing-Hua Jiao^a ; ^{huangcaiguo@hotmail.com}
• 关键词：尾-d-Glucosyl-(1&ndash ; 4)-伪-l-thevetosides of 17尾-digitoxigenin (GHSC-73) ; HepG2 ; Apoptosis-inducing factor (AIF) ; Mitochondrial membrane potential (螖唯m) ; Caspase-3 ; Apoptosis
• 刊名：Experimental and Toxicologic Pathology
• 出版年：2012
• 期刊代码：128_09402993
• 类别：med
• 出版时间：July, 2012
• 卷：64
• 期：5
• 页码：403-410
• 文件大小：912 K

摘要

尾-d-Glucosyl-(1-4)-伪-l-thevetosides of 17尾-digitoxigenin (GHSC-73) is a cardiac glycoside isolated from the seeds of Cerbera manghas L. GHSC-73 reduced viability of HepG2 cells in a time- and dose-dependent manner without decreasing the viability of Chang human liver cells and Swiss albino 3T3 fibroblasts, induced efficiently stimulated apoptosis in HepG2 cells as evidenced by DNA fragmentation, annexin V/PI binding assay and DAPI staining. This apoptotic process was accompanied by the activation of the effector caspase-3, the loss of mitochondrial membrane potential (螖唯_m) and translocation of AIF from the mitochondrion to the nucleus in HepG2 cells. In addition, a broad-spectrum caspase inhibitor (z-VAD-fmk) tested in this experiment partially prevent HepG2 cells from GHSC-73-induced cell death, but did not affect translocation of AIF from the mitochondrion to the nucleus after GHSC-73 treatment. Our results firstly show that GHSC-73 inhibits the growth of HepG2 cells through caspase-dependent and -independent apoptosis pathways.