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Inhibitory effects of epigallocatechin-3-O-gallate on serum-stimulated rat aortic smooth muscle cells via nuclear factor-κB down-modulation
- Inhibitory effects of epigallocatechin-3-O-gallate on serum-stimulated rat aortic smooth muscle cells via nuclear factor-κB down-modulation
- Han D.-W.; Lim H.R.; Baek H.S.; Lee M.H.; Lee S.J.; Hyon S.-H.; Park J.-C.
- Ewha Authors
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- Journal Title
- Biochemical and Biophysical Research Communications
- vol. 345, no. 1, pp. 148 - 155
- SCI; SCIE; SCOPUS
- The abnormal growth of vascular smooth muscle cells (VSMCs) plays an important role in vascular diseases, including atherosclerosis and restenosis after angioplasty. Although (-)-epigallocatechin-3-O-gallate (EGCG) has antiproliferative effects on various cells, relatively a little is known about precise mechanisms of the inhibitory effects of EGCG on SMCs. In this study, the inhibitory effects of EGCG on attachment, proliferation, migration, and cell cycle of rat aortic SMCs (RASMCs) with serum stimulation were investigated. Also, the involvement of nuclear factor-κB (NF-κB) during these inhibitions by EGCG was examined. EGCG treatment resulted in significant (p < 0.05) inhibition in attachment and proliferation of RASMCs induced by serum. While non-treated RASMCs migrated into denuded area in response to serum and showed essentially complete closure after 36 h, EGCG-treated cells covered only 31% of the area even after 48 h of incubation. Furthermore, EGCG treatment resulted in an appreciable cell cycle arrest at both G0/G1- and G2/M-phases. The immunoblot analysis revealed that the constitutive expression of NF-κB/p65 nuclear protein in RASMCs was lowered by EGCG in both the cytosol and the nucleus in a dose-dependent manner. These results suggest that the EGCG-caused inhibitory effects on RASMCs may be mediated through NF-κB down-modulation. © 2006 Elsevier Inc. All rights reserved.
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