AIM:To observe the effects of sargentgloryvine stem extracts (SSE) on the hepatoma cell line HepG-2 in vitro andin vivo and determine its mechanisms of action.METHODS:Cultured HepG-2 cells treated with SSE were analys...AIM:To observe the effects of sargentgloryvine stem extracts (SSE) on the hepatoma cell line HepG-2 in vitro andin vivo and determine its mechanisms of action.METHODS:Cultured HepG-2 cells treated with SSE were analysed by 3-(4,5-Dimethyl-thiazol-2-yl)-2,5Diphenyltetrazolium bromide and clone formation assay.The cell cycle and apoptosis analysis were conducted by flow cytometric,TdT-Mediated dUTP Nick End Labeling and acridine orange/ethidium bromide staining methods,and protein expression was examined by both reverse transcriptase-polymerase chain reaction and Western blotting.The pathological changes of the tumor cells were observed by haematoxylin and eosin staining.Tumor growth inhibition and side effects were determined in a xenograft mouse model.RESULTS:SSE treatment could not only inhibit HepG-2 cell proliferation in a doseand time-dependent manner but also induce apoptosis and cell cycle arrest at the S phase.The number of colonies formed by SSEtreated tumor cells was fewer than that of the controls (P<0.05).SSE induced caspase-dependent apoptosis accompanied by a significant decrease in Bcl-xl and Mcl-1 and elevation of Bak expression (P<0.05).Tumor necrosis factor α in the xenograft tumor tissue and the liver functions of SSE-treated mice showed no significant changes at week 8 compared with the control group (P>0.05).Systemic administration of SSE could inhibit the HepG-2 xenograft tumor growth with no obvious toxic side effects on normal tissues.CONCLUSION:SSE can induce apoptosis of HepG-2 cells in vitro and in vivo through decreasing expression of Bcl-xl and Mcl-1 and increasing expression of Bax.展开更多
基金Supported by National Science and Technology Key Project for the Development of New Drugs in China,No. 2009ZX09103-422
文摘AIM:To observe the effects of sargentgloryvine stem extracts (SSE) on the hepatoma cell line HepG-2 in vitro andin vivo and determine its mechanisms of action.METHODS:Cultured HepG-2 cells treated with SSE were analysed by 3-(4,5-Dimethyl-thiazol-2-yl)-2,5Diphenyltetrazolium bromide and clone formation assay.The cell cycle and apoptosis analysis were conducted by flow cytometric,TdT-Mediated dUTP Nick End Labeling and acridine orange/ethidium bromide staining methods,and protein expression was examined by both reverse transcriptase-polymerase chain reaction and Western blotting.The pathological changes of the tumor cells were observed by haematoxylin and eosin staining.Tumor growth inhibition and side effects were determined in a xenograft mouse model.RESULTS:SSE treatment could not only inhibit HepG-2 cell proliferation in a doseand time-dependent manner but also induce apoptosis and cell cycle arrest at the S phase.The number of colonies formed by SSEtreated tumor cells was fewer than that of the controls (P<0.05).SSE induced caspase-dependent apoptosis accompanied by a significant decrease in Bcl-xl and Mcl-1 and elevation of Bak expression (P<0.05).Tumor necrosis factor α in the xenograft tumor tissue and the liver functions of SSE-treated mice showed no significant changes at week 8 compared with the control group (P>0.05).Systemic administration of SSE could inhibit the HepG-2 xenograft tumor growth with no obvious toxic side effects on normal tissues.CONCLUSION:SSE can induce apoptosis of HepG-2 cells in vitro and in vivo through decreasing expression of Bcl-xl and Mcl-1 and increasing expression of Bax.
