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논문 기본 정보

자료유형
학술저널
저자정보
Young-Eun Cho (안동대학교) Jee-Eun Choi (안동대학교) Jahangir Alam (안동대학교) Man-Hyo Lee (경북바이오산업연구원) Ho-Yong Sohn (안동대학교) John H. Beattie (Rowett Research Institute) In-Sook Kwun (안동대학교)
저널정보
한국영양학회 Nutrition Research and Practice Nutrition Research and Practice Vol.2 No.2
발행연도
2008.6
수록면
74 - 79 (6page)

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Zinc plays a protective role in anti-atherosclerosis but the clear mechanism has not been proposed yet. In the present study, we evaluated whether zinc modulates atherosclerotic markers, VACM-1 and ICAM-1 and cell viability both in endothelial cells in vitro and mouse aortic cell viability ex vivo. In study 1, as in vitro model, endothelial EA.hy926 cells were treated with TNFα for 5 hours for inducing oxidative stress, and then treated with Zn-adequacy (15 μM Zn) or Zn-deficiency (0 μM Zn) for 6 hours. Pro-atherosclerosis factors, VCAM-1 and ICAM-1 mRNA expression and cell viability was measured. In study 2, as ex vivo model, mouse aorta ring was used. Mourse aorta was removed and cut in ring then, cultured in a 96-well plate. Aortic ring was treated with various TNFα (0-30 ㎎/㎖) and intracellular zinc chelator, N, N, N′, N′, -tetrakis (2-pyridylmethyl) ethylenediamine (TPEN, 0-30 μM) for cellular zinc depletion for 2 days and then cell viability was measured. The results showed that in in vitro study, Zn-adequate group induced more VCAM-1 & ICAM-1 mRNA expression than Zn-deficient group during 6-hour zinc treatment post-5 hour TNF-α treatment, unexpectedly. These results might be cautiously interpreted that zinc would biologically induce the early expression of anti-oxidative stress through the increased adhesion molecule expression for reducing atherosclerotic action, particularly under the present 6-hour zinc treatment. In ex vivo, mouse aortic ring cell viability was decreased as TNF-α and TPEN levels increased, which suggests that mouse aortic blood vessel cell viability was decreased, when oxidative stress increases and cellular zinc level decreases. Taken together, it can be suggested that zinc may have a protective role in anti-atherosclerosis by cell viability in endothelial cells and aorta tissue. Further study is needed to clarify how pro-atherosclerosis molecule expression is modulated by zinc.

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Abstract
Introduction
Materials and Methods
Results
Discussion
Literature cited

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UCI(KEPA) : I410-ECN-0101-2012-594-004461176