摘要
AIM: To study the mechanism of cytotoxicity of a new active 5-alkyl resorcinol [1, 3-dihydroxy-5- (tridec-4’, 7’ -dienyl) benzene] isolated from Lithraea molleoides leaves on liver tumor cells. METHODS: Human hepatocarcinoma cell lines (HepG2 and Hep3B) in culture were treated with inhibitory concentrations, 50% of the compound, for 24 h. The induction of apoptosis was detected in treated cells by analysis of DNA fragmentation, DNA content, and acridine orange and propidium iodide staining. RESULTS: After 24 h of 5-alkyl resorcinol treatment, both cell lines showed: (1) the typical morphological alterations of apoptosis; (2) DNA fragmentation, detected by laddering and appearance of a subG0 population by flow cytometry; and (3) condensed and fragmented nuclei by acridine orange-propidium iodide staining. CONCLUSION: Based on the results, this compound exerts its cytotoxic effect in both hepatocellular cell lines through apoptotic cell death. For Hep3B, cells with mutated p53 and Fas, apoptosis would proceed by p53- or Fas-independent pathways.
AIM： To study the mechanism of cytotoxicity of a new active 5-alkyl resorcinol [1, 3-dihydroxy-5- （tridec-4＇, 7＇ -dienyl） benzene] isolated from Lithraea molleoides leaves on liver tumor cells. METHODS： Human hepatocarcinoma cell lines （HepG2 and Hep3B） in culture were treated with inhibitory concentrations, 50% of the compound, for 24 h. The induction of apoptosis was detected in treated cells by analysis of DNA fragmentation, DNA content, and acridine orange and propidium iodide staining. RESULTS： After 24 h of 5-alkyl resorcinol treatment, both cell lines showed： （1） the typical morphological alterations of apoptosis, （2） DNA fragmentation, detected by laddering and appearance of a subG0 population by flow cytometry, and （3） condensed and fragmented nuclei by acridine orange-propidium iodide staining. CONCLUSION： Based on the results, this compound exerts its cytotoxic effect in both hepatocellular cell lines through apoptotic cell death. For Hep3B, cells with mutated p53 and Fas, apoptosis would proceed by p53- or Fas-independent pathways.
基金
Supported by research grants from Agencia Nacional de Promocion Cientifi ca y Tecnologica of Argentina, No.PICT 8355, and from Universidad de Buenos Aires, No.B033 and B036
作者简介
Correspondence to： Lucia Cavallaro, Catedra de Virologia, Facultad de Farmacia y Bioquimica, Universidad de Buenos Aires, Junin 956 4th floor （1113） Buenos Aires, Argentina. lbarbini@ffyb.uba.ar Telephone： ＋54-11-49648264 Fax： ＋54-11-45083645
