間歇性缺氧對心肌擴張及心肌凋亡之探討：加鐵氧化傷害加乘長期間歇性缺氧誘發心肌擴張及凋亡研究(I); 探討短暫和長期間歇性缺氧對心臟細胞凋亡及存活訊息途徑之影響差異(II)

中山醫學大學機構典藏 CSMUIR > 醫學科技學院 > 物理治療學系暨碩士班 > 研究計劃 > Item 310902500/2944

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/2944

Title:	間歇性缺氧對心肌擴張及心肌凋亡之探討：加鐵氧化傷害加乘長期間歇性缺氧誘發心肌擴張及凋亡研究(I);探討短暫和長期間歇性缺氧對心臟細胞凋亡及存活訊息途徑之影響差異(II) Effect of Intermittent Hypoxia on Cardiac Hypertrophy and Apoptosis---Synergistic Effect of Iron Oxidative (I);Effect of Short-Term VS Long-Term Intermittent (II)
Authors:	李信達;黃志揚 Li, Sin-Der;Huang, Chih-Yang
Contributors:	中山醫學大學物理治療學系
Keywords:	Cardiac fibrosis;Cell apoptosis;High altitude;Fas pathway;Time course
Date:	2006
Issue Date:	2010-11-29T04:49:04Z (UTC)
Abstract:	Background. Short-term versus long-term intermittent hypoxia had been shown to exert cardiac protective versus deleterious effects. It is unclear if short-term versus long-term intermittent hypobaric hypoxic challenges exert opposite effects on Fas death receptor-dependent apoptotic pathway in rat hearts. Methods. Seventy-two Sprague-Dawley rats were randomized assigned into two groups: first, short-term intermittent hypobaric hypoxia (STIHH)-normobaric normoxia (n=12), hypobaric hypoxia (380 mmHg, 12% O2, 8 hrs/day) for 1 day (n=12), and for 4 days (n=12) and second, long-term intermittent hypobaric hypoxia (LTIHH)-normobaric normoxia (n=12), hypobaric hypoxia for 1 week (n=12) and 2 weeks (n=12). After STIHH or LTIHH challenge, Fas receptor-related pathway and histopathological analysis in the excised left ventricle was determined by Western blotting, RT-PCR, Hematoxylin-eosin staining, and Masson trichrome staining. Results. Pro-apoptotic Fas death receptors and TNFalphamRNA were significantly decreased after STIHH and Fas ligand, Fas associated death domain (FADD), activated caspase 8 were not changed after STIHH whereas Fas receptor, TNFalpha, FADD, and caspase 8 were increased after LTIHH. In addition, cardiomyocyte disarray and fibrosis were observed in 1 week LTIHH as well as cardiac hypertrophy and more severe disarray and fibrosis were observed in 2 week LTIHH. Conclusions. STIHH appeared to exert protective effects on hearts such as downregulation of TNFalphamRNA and Fas receptor whereas LTIHH appeared to exert deleterious and pro-apoptotic effects such as upregulation of TNFalphaand Fas-mediated apoptotic pathways and lead to cardiac fibrosis, which imply that cardiac protective or pro-apoptotic effect exerted by intermittent hypobaric hypoxia is tightly time-course dependent.
URI:	https://ir.csmu.edu.tw:8080/handle/310902500/2944
Appears in Collections:	[物理治療學系暨碩士班] 研究計劃

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