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Gallotannin regulates apoptosis and COX-2 expression via Akt and p38kinase pathway in human lung cancer cell line, A549

Animal Cells and Systems 2012년 16권 5호 p.366 ~ 375
유선미, 권은정, 정기화, 김광훈, 조홍식, 김송자,
소속 상세정보
유선미 ( Yu Seon-Mi ) - Kongju National University College of Natural Sciences Department of Biological Sciences
권은정 ( Gweon Eun-Jeong ) - Kongju National University College of Natural Sciences Department of Biological Sciences
정기화 ( Chung Ki-Wha ) - Kongju National University College of Natural Sciences Department of Biological Sciences
김광훈 ( Kim Kwang-Hoon ) - Kongju National University College of Natural Sciences Department of Biological Sciences
조홍식 ( Cho Hong-Sik ) - University of Tennessee Health Science Center
김송자 ( Kim Song-Ja ) - Kongju National University College of Natural Sciences Department of Biological Sciences

Abstract


Gallotannin (GT) is derived from plant poly phenol and is associated with biological actions in a wide range of cells. In this study, we evaluated the effect of GT on apoptosis and cyclooxygenase-2 (COX-2) expression and attempted to shed light on the mechanism of action in A549 human lung carcinoma cells. We found that GT dramatically induced apoptosis as demonstrated by expression of p53 and active caspase-3 via western blot analysis and fragmented DNA as detected by DNA fragmentation and DAPI staining. We also observed that GT significantly causes COX-2 expression in a dose-dependent manner determined by western blot analysis. Phosphorylation of Akt and p38 was considerably increased by GT in A549 human lung carcinoma cells. Inhibition of Akt and p38kinase with LY294002 or SB203580 suppressed GT-induced apoptosis and COX-2 expression. Furthermore, we have shown that prevention of COX-2 with NS398 or indomethacin does not any effects on apoptosis induced by GT. Taken together, our present results suggest that GT regulates apoptosis and COX-2 expression through Akt and p38kinase pathway in A549, human lung carcinoma cells.

키워드

gallotannin (GT); A549; apoptosis; cyclooxygenase-2 (COX-2); Akt; p38kinase

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