Please use this identifier to cite or link to this item: https://doi.org/10.1016/S0304-3835(00)00391-8
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dc.titleSalvia miltiorrhiza inhibits cell growth and induces apoptosis in human hepatoma HepG2 cells
dc.contributor.authorLiu, J.
dc.contributor.authorShen, H.-M.
dc.contributor.authorOng, C.-N.
dc.date.accessioned2014-12-01T06:56:46Z
dc.date.available2014-12-01T06:56:46Z
dc.date.issued2000-05-29
dc.identifier.citationLiu, J., Shen, H.-M., Ong, C.-N. (2000-05-29). Salvia miltiorrhiza inhibits cell growth and induces apoptosis in human hepatoma HepG2 cells. Cancer Letters 153 (1-2) : 85-93. ScholarBank@NUS Repository. https://doi.org/10.1016/S0304-3835(00)00391-8
dc.identifier.issn03043835
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/113638
dc.description.abstractSalvia miltiorrhiza (SM) is a traditional Chinese herbal medicine, commonly used to treat liver diseases in China for centuries. Several earlier studies have indicated that SM exhibits anti-tumor properties, but its mechanism remains to be elucidated. In this study, we evaluated the molecular mechanism of SM in a human hepatoma cell line, HepG2. Our results show that SM exerted clear cytotoxic effects, and strongly inhibited the proliferation of HepG2 cells. It was also observed that SM treatment caused apoptotic cell death as evaluated by: (a), morphological changes by using acridine orange/ethidium bromide staining; (b), DNA fragmentation by TdT-mediated dUTP nick end labeling (TUNEL); and (c), sub-G1 cell analysis. Furthermore, depletion of intracellular glutathione (GSH) and reduction of mitochondrial membrane potential were found to be involved in the initiation of apoptosis by SM. Copyright (C) 2000 Elsevier Science Ireland Ltd.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/S0304-3835(00)00391-8
dc.sourceScopus
dc.subjectGlutathione
dc.subjectHerbal medicine
dc.subjectMitochondrial membrane potential
dc.subjectProliferation
dc.subjectSub-G1 cell
dc.subjectTdT-mediated dUTP nick end labeling
dc.typeArticle
dc.contributor.departmentCOMMUNITY,OCCUPATIONAL & FAMILY MEDICINE
dc.description.doi10.1016/S0304-3835(00)00391-8
dc.description.sourcetitleCancer Letters
dc.description.volume153
dc.description.issue1-2
dc.description.page85-93
dc.description.codenCALED
dc.identifier.isiut000166661600013
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