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Pro-Apoptotic Effect of Mori Cortex Radicis in A549 Lung Cancer Cells  

Bae Oh-Sung (Dong Bang University of Graduate School)
Yoo Yeong-Min (Department of Oriental Pathology, College of Oriental Medicine, Sangji University)
Lee Seon-Goo (Department of Oriental Pathology, College of Oriental Medicine, Sangji University)
Publication Information
Journal of Physiology & Pathology in Korean Medicine / v.19, no.6, 2005 , pp. 1563-1567 More about this Journal
Abstract
Mori Cortex Radicis is distributed in Northwestern China, northern Asia, northern Europe, North America, and Korea. This extracts drops sugar in bloods and inhibits cyclic AMP phophodiesterase. In this study, we investigated whether Mori Cortex Radicis would cause apoptotic death of A549 lung cancer cells. To examine the apoptotic effect of Mori Cortex Radicis, cytotoxicity assay, DNA fragmentation analysis, caspase-3 activity assay, and Western blotting for caspase-3, caspase-9 and poly(ADP-ribose) polymerase (PARP) and cytochrome c were performed. Treatment of cells with Mori Cortex Radicis was shown to induce cell death in a dose-dependent manner. DNA fragmentation was made in response to Mori Cortex Radicis. The active fragments of caspase-3, caspase-9 and PARP were almost completely induced and cytochrome c was released following exposure to Mori Cortex Radicis. To elucidate the apoptotic mechanisms, RT-PCR and Western blot analyses for the expression of Bcl-2, Bu and Cox-2 were carried out. Treatment with Mori Cortex Radicis was expressed the reduction of Bcl-2 and Cox-2 and the induction of Bax. Especially p21 and p53 were increased prior to untreated control, while cyclin E and cyclin D1 decreased in the cytosol. These results suggest that the effect Mori Cortex Radicis is associated with the cell cycle arrest and pro-apoptotic cell death in A549 lung cancer cells.
Keywords
Mori Cortex Radicis; A549 lung cancer cells; Caspase-3; Bax; Cox-2;
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