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Sasanquasaponin from Camellia oleifera Abel. induces apoptosis via Bcl-2, Bax and caspase-3 activation in HepG2 cells

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The present study aimed to elucidate the molecular mechanisms underlying the induction of cytotoxic effects by sasanquasaponin (SQS) in HepG2 cells. Following SQS treatment, time and dosedependent increases in the apoptotic rate were observed. The induction of cell death by SQS mainly occurs via programmed cell death, as indicated by Annexin Vfluorescein isothiocyanate and propidium iodide staining, where up to 30% apoptotic cells were detected following 12 h SQS treatment. Reverse transcriptionpolymerase chain reaction analysis demonstrated that SQS treatment upregulated Bcell lymphoma2 (Bcl2)associated x protein and caspase3 mRNA expression and downregulated Bcl2 mRNA expression. Greater alterations in Bax, Bcl2 and caspase3 expression were observed with increasing treatment duration. The decrease in Bcl2, increase in Bax and, finally, the activation of caspase3 in HepG2 cells indicated that the apoptotic process induced by SQS was irreversible. The results of the present study therefore suggested that SQS induced HepG2 cell apoptosis via the activation of mitochondrial apoptotic pathways.
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Document Type: Research Article

Affiliations: 1: Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China 2: College of Pharmacy, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China

Publication date: August 1, 2015

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  • Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
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