Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/69355
標題: Effects of long-term intermittent hypoxia on mitochondrial and Fas death receptor dependent apoptotic pathways in rat hearts
作者: Lee, S.D.
Kuo, W.W.
Lin, J.A.
Chu, Y.F.
Wang, C.K.
Yeh, Y.L.
Wang, S.G.P.
Liu, J.Y.
Chang, M.H.
Huang, C.Y.
關鍵字: cardiac
Fas death receptor
hypoxia
mitochondrial dependent pathway
high-altitude hypoxia
cytochrome-c
nocturnal hypoxemia
disease
myocardium
activation
caspase-3
family
bnip3
bcl-2
期刊/報告no:: International Journal of Cardiology, Volume 116, Issue 3, Page(s) 348-356.
摘要: Background: It is unclear whether the cardiac mitochondrial dependent apoptotic pathways and Fas death receptor dependent apoptotic pathways will be induced by long-term intermittent hypoxia. Methods: Twenty-seven Sprague-Dawley rats were randomly assigned into three groups: normoxia, long-term intermittent hypoxia (12% 02, 8 h/day) for 4 weeks (4WLTIH) and for 8 weeks (8WLTIH). Histological analysis, Western blotting and RT-PCR in the three groups were performed on tissue from the excised left ventricle. Results: Mitochondrial dependent pro-apoptotic pathway, BNIP3, caspase 9, and caspase 3, and the Fas death receptor dependent proapoptotic pathway, Fas, caspase 8, and caspase 3 were all significantly increased after 4WLTIH and even further enhanced after 8WLTIH. In addition, mitochondrial related anti-apoptotic proteins, Bcl2, its upstream phosphorylated protein kinase B (Akt), and the mitochondrial key oxidative enzyme, cytochrome c oxidase, were all decreased after 4WLTIH and further reduced after 8WLTIH. Conclusions: The mitochondrial dependent apoptotic pathways and Fas death receptor dependent apoptotic pathways in rat hearts were both activated by long-term intermittent hypoxia. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
URI: http://hdl.handle.net/11455/69355
ISSN: 0167-5273
文章連結: http://dx.doi.org/10.1016/j.ijcard.2006.03.064
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