마이크로네시아 해조류 Pylaiella littoralis 추출물의 항증식활성 효과

Abstract

This study confirmed that five tumorigenic cells, AGS, DU145, SK-HEP, NCI-H1299 and HT-29 cells were treated with Pylaiella littoralis extract (PLE) to determine anti-proliferative activity. The highest inhibitory activity of PLE showed in HT-29 cells and exhibited no cytotoxic effect with increasing concentration for normal cells and inhibited cell growth of HT-29 cells depending on concentration and time. Also, we identified that growth inhibition rate on HT-29 cells of PLE was associated by as nuclear condensation, apoptotic body formation, DNA fragmentation and sub-G1 DNA accumulation in HT-29 cells. PLE also induced increase of mitochondrial membrane permeabilization compare with untreated PLE and exhibited decreasing Bcl-2 protein, increasing Bax protein, activating Caspase-3 and PARP expressions via caspases pathway. Indeed, PLE increased expression of phosphorylation of JNK, P38 and ERK and attenuated specific inhibitors of JNK, P38 and ERK via MAPKs pathway. In conclusion, this study demonstrated that PLE could inhibit the proliferation of HT-29 cells by caspases and MAPKs pathways involving the induction of apoptosis.HT-29 cells and exhibited no cytotoxic effect with increasing concentration for normal cells and inhibited cell growth of HT-29 cells depending on concentration and time. Also, we identified that growth inhibition rate on HT-29 cells of PLE was associated by as nuclear condensation, apoptotic body formation, DNA fragmentation and sub-G1 DNA accumulation in HT-29 cells. PLE also induced increase of mitochondrial membrane permeabilization compare with untreated PLE and exhibited decreasing Bcl-2 protein, increasing Bax protein, activating Caspase-3 and PARP expressions via caspases pathway. Indeed, PLE increased expression of phosphorylation of JNK, P38 and ERK and attenuated specific inhibitors of JNK, P38 and ERK via MAPKs pathway. In conclusion, this study demonstrated that PLE could inhibit the proliferation of HT-29 cells by caspases and MAPKs pathways involving the induction of apoptosis.