Eccentric cardiac hypertrophy was induced by long-term intermittent hypoxia in rats

doi:10.1113/expphysiol.2006.036590

中山醫學大學機構典藏 CSMUIR > 口腔醫學院 > 口腔醫學研究所 > 期刊論文 > Item 310902500/15673

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Title:	Eccentric cardiac hypertrophy was induced by long-term intermittent hypoxia in rats
Authors:	Chen, Li-Mien Kuo, Wei-Wen Yang, Jaw-Ji Wang, Shyi-Gang P. Yeh, Yu-Lan Tsai, Fuu-Jen Ho, Ying-Jui Chang, Mu-Hsin Huang, Chih-Yang Lee, Shin-Da
Contributors:	中山醫大口腔科學研究所
Date:	2007-03-01
Issue Date:	2016-08-09T06:25:13Z (UTC)
Abstract:	It is unclear whether cardiac hypertrophy and hypertrophy-related pathways will be induced by long-term intermittent hypoxia. Thirty-six Sprague-Dawley rats were randomly assigned into three groups: normoxia, and long-term intermittent hypoxia (12% O(2), 8 h per day) for 4 weeks (4WLTIH) or for 8 weeks (8WLTIH). Myocardial morphology, trophic factors and signalling pathways in the three groups were determined by heart weight index, histological analysis, Western blotting and reverse transcriptase-polymerase chain reaction from the excised left ventricle. The ratio of whole heart weight to body weight, the ratio of left ventricular weight to body weight, the gross vertical cross-section of the heart and myocardial morphological changes were increased in the 4WLTIH group and were further augmented in the 8WLTIH group. In the 4WLTIH group, tumour necrosis factor-alpha(TNFalpha), insulin-like growth factor (IGF)-II, phosphorylated p38 mitogen-activated protein kinase (P38), signal transducers and activators of transcription (STAT)-1 and STAT-3 were significantly increased in the cardiac tissues. However, in the 8WLTIH group, in addition to the above factors, interleukin-6, mitogen-activated protein kinase (MEK)5 and extracellular signal-regulated kinase (ERK)5 were significantly increased compared with the normoxia group. We conclude that cardiac hypertrophy associated with TNFalpha and IGF-II was induced by intermittent hypoxia. The longer duration of intermittent hypoxia further activated the eccentric hypertrophy-related pathway, as well as the interleukin 6-related MEK5-ERK5 and STAT-3 pathways, which could result in the development of cardiac dilatation and pathology.
URI:	http://dx.doi.org/10.1113/expphysiol.2006.036590 https://ir.csmu.edu.tw:8080/ir/handle/310902500/15673
Relation:	Exp Physiol. 2007 Mar;92(2):409-416.
Appears in Collections:	[口腔醫學研究所] 期刊論文

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