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논문 기본 정보

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학술저널
저자정보
Jung, Woo-Sang (Department of Cardiovascular and Neurologic Diseases, Hospital of Oriental Medicine, Kyung Hee Medical Center, Kyung Hee University) Cho, Jin-Gu (Department of Molecular Biology & Institute of Nanosensor and Biotechnology, BK21 Graduate Program for RNA Biology, Dankook University) In, Kyung-Min (Department of Molecular Biology & Institute of Nanosensor and Biotechnology, BK21 Graduate Program for RNA Biology, Dankook University) Kim, Jong-Min (Department of Molecular Biology & Institute of Nanosensor and Biotechnology, BK21 Graduate Program for RNA Biology, Dankook University) Cho, Ki-Ho (Department of Cardiovascular and Neurologic Diseases, Hospital of Oriental Medicine, Kyung Hee Medical Center, Kyung Hee University) Park, Jung-Mi (Department of Stroke and Neurological Disorders Center, East-West Neo Medical Center, Kyung Hee University) Moon, Sang-Kwan (Department of Cardiovascular and Neurologic Diseases, Hospital of Oriental Medicine, Kyung Hee Medical Center, Kyung Hee University) Kim, Kyung-Wook (Department of Cardiovascular and Neurologic Diseases, Hospital of Oriental Med) Park, Seong-Uk Pyee, Jae-Ho Park, Sang-Gyu Jeong, Yoon-Hwa Park, Heon-Yong Ko, Chang-Nam
저널정보
한국통합생물학회 Animal cells and systems Animal cells and systems 제14권 제4호
발행연도
2010.1
수록면
275 - 282 (8page)

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Chunghyul-dan (CHD) is a combinatorial drug known to exert anti-inflammatory effects in endothelial cells. In this study, we employed global transcriptional profiling using cDNA microarrays to identify molecular mechanisms responsible for the anti-inflammatory activity of CHD in endothelial cells. An analysis of the microarray data revealed that transcript levels of monocyte chemotactic protein-1 (MCP-1), vascular cell-adhesion molecule-1 (VCAM-1) and activated leukocyte cell-adhesion molecule were dramatically altered in CHD-treated endothelial cells. These changes in gene expression were confirmed by RT-PCR, Western blotting and ELISA. Chronic CHD treatment also appeared to decrease MCP-1 secretion, probably as a result of decreased MCP-1 expression. In addition, we determined that chronic CHD treatment inhibited lipopolysaccharide-stimulated adhesion of THP-1 leukocytes to endothelial cells. The inhibitory effect of CHD on LPS-stimulated adhesion resulted from downregulation of VCAM-1 expression. Transmigration of THP-1 leukocytes through endothelial cells was also inhibited by chronic CHD treatment. In conclusion, CHD controls a variety of inflammatory activities by regulating MCP-1 and VCAM-1 gene expression.

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