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( Hao Jin ),( Wen Yi Jiang ),( Jin Huai Chi ),( Sung Hee Lee ),( Jae Hoon Jahng ),( Young Bum Cho ),( Geom Seog Seo ) 대한내과학회 2014 대한내과학회 추계학술발표논문집 Vol.2014 No.1
Background: A role for autophagy, a conserved cellular response to stress, has recently been demonstrated in human cancers. Heme oxygenase-1 (HO-1) is a stress-inducible enzyme with anti-apoptotic property. In this study, we investigated the association between isoliquiritigenin (ISQ) and autophagy in HCT-116 cells. In addition, we determined whether the anti-apoptotic effects are mediated by HO-1-dependent autophagy. Methods: The protein expression of HO-1, LC3B-II, ATG5, ATG7, Benclin-1, PARP were analyzed by western blot analysis. Autophagy was assessed by acridine orange staining, immunofl uorescence (LC3 puncta). Knock-down of HO-1 expression was achieved with siRNA. Results: ISQ signifi cant induced LC3B-II, Beclin-1, ATG5, ATG7, PARP cleavage, expression compared to control values. Treatment with bafi lomycin A1 (BaF), autophagy inhibitor, significantly enhanced ISQ-induced accumulation of the autophagosomal marker LC3B-II and PARP cleavage. ISQ induce autophagy which inhibits against ISQ-induced apoptosis in HCT-116 cells. Furthermore, HO-1 knockdown by siRNA abolished the effects of anti-apoptotic and decreased LC3-II/LC3-I ratio in HCT-116 cells. The protective role of autophagy was dependent on HO-1 in HCT-116. Conclusions: Our results demonstrated that ISQ induce autophagy which is mediated by induction of HO-1 expression. ISQ-induced autophagy followed by apoptosis in HCT-116 cells.