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Chaga mushroom (Inonotus obliquus) induces G0/G1 arrest and apoptosis in human hepatoma HepG2 cells

World Journal of Gastroenterology 2008年第4期14卷 511-517页

作者： Myung-Ja Youn Jin-Kyung Kim Seong-Yeol park Yunha Kim Se-Jin Kim Jin Seok Lee Kyu Yun Chai Hye-Jung Kim Ming-Xun Cui Hong Seob So Ki-Young Kim raekil park Vestibulocochlear Research Center Wonkwang University School of MedicineJeonbuk Korea College of Human Environmental Science -Wonkwang-University Jeonbuk Korea Department of Bionanochemistry College of Natural Science Wonkwang University JeonbukKorea Department of Family Medicine WonkwangUniversity Hospital Wonkwang University Jeonbuk Korea

AIM: To investigate the anti-proliferative and apoptotic effects of Chaga mushroom (Inonotus obliquus) water extract on human hepatoma cell lines,HepG2 and Hep3B cells. METHODS: The cytotoxicity of Chaga extract was screened by 3-4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide (MTT) assay. Morphological observation,flow cytometry analysis,Western blot were employed to elucidate the cytotoxic mechanism of Chaga extract. RESULTS: HepG2 cells were more sensitive to Chaga extract than Hep3B cells,as demonstrated by markedly reduced cell viability. Chaga extract inhibited the cell growth in a dose-dependent manner,which was accompanied with G0/G1-phase arrest and apoptotic cell death. In addition,G0/G1 arrest in the cell cycle was closely associated with down-regulation of p53,pRb,p27,cyclins D1,D2,E,cyclin-dependent kinase (Cdk) 2,Cdk4,and Cdk6 expression. CONCLUSION: Chaga mushroom may provide a new therapeutic option,as a potential anticancer agent,in the treatment of hepatoma.

关键词： Inonotus obliquus, Cell cycle G0/G1 arrest Apoptosis

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Berberine-Induced Apoptosis in Human Glioblastoma T98G Cells Is Mediated by Endoplasmic Reticulum Stress Accompanying Reactive Oxygen Species and Mitochondrial Dysfunction

Berberine-Induced Apoptosis in Human Glioblastoma T98G Cells...

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中国抗癌协会神经肿瘤专业委员会第八届学术会议

作者： Ki Seong EOM Hyung-Jin KIM Hong-Seob SO raekil park Tae Young KIM Department of Neurosurgery Wonkwang University Department of Microbiology School of MedicineWonkwang University VestibuloCochlear Reserch Center and Department of Microbiology School of MedicineWonkwang University

Berberine has a wide range of biochemical and pharmacologic effects,including antitumor activity,but the mechanisms involved in berberine-induced apoptosis remain *** purpose of the present study was to investigate the changes in oxidative stress and endoplasmic reticulum（ER）-related molecules,which are closely associated with cell death-signaling transduction pathways,in human glioblastoma T98G cells treated with *** significantly decreased the cell viability of T98G cells in a dose-dependent *** increased the production of reactive oxygen species（ROS） and level of intracellular *** induced ER stress as evidenced by the detection of ER stress-associated molecules such as phosphorylated protein kinaselike ER kinase,eukaryotic translation initiation factor-2a,glucose-regulated protein 78/immunoglobulin heavy chain-binding protein,and CCAAT/enhancer-binding protein（C/EBP）-homologous protein/growth arrest and DNA damage-inducible gene 153,which was associated with the activation of ***,the administration of the antioxidants,N-acetylcysteine and glutathione,reversed berberine-induced *** also markedly enhanced apoptosis in T98G cells through the induction of a higher ratio of Bax/Bcl-2 proteins,disruption of the mitochondrial membrane potential,activation of caspase-9 and-3,and cleavage of the poly（ADP-ribose） polymerase（PARP）.The inhibition of ER stress using salubrinal led to an increased the level of Bcl-2,whereas the level of Bax,cleavage of procaspase-9 and-3,and PARP were decreased when compared with cells treated with berberine alone,indicating that berberine-induced apoptosis is associated with mitochondrial *** results demonstrate that berberine induces apoptosis via ER stress through the elevation of ROS and mitochondrial-dependent pathway in human glioblastoma T98G cells.

关键词： berberine endoplasmic reticulum glioblastoma reactive oxygen species mitochondria

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