Hyperthermic preconditioning protects astrocytes from ischemia/reperfusion injury by up-regulation of HIF-1 alpha expression and binding activity
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摘要It has been demonstrated that hypoxia-inducible factor-1 alpha (HIF-1 alpha) mediates ischemic tolerance induced by hypoxia/ischemia or pharmacological preconditioning. In addition, preconditioning stimuli can be cross-tolerant, safeguarding against other types of injury. We therefore hypothesized HIF-1 alpha might also be associated with ischemic tolerance induced by hyperthermic preconditioning. In the present study, we demonstrated for the first time that 6 h of hyperthermia (38 degrees C or 40 degrees C) could induce a characteristic "reactive" morphology and a significant increase in the expression of bystin in astrocytes. We also showed that pre-treatment with 6 h of hyperthermia resulted in a significant increase in cell viability and a remarkable decrease in lactate dehydrogenase (LDH) release and apoptosis development in the astrocytes that were exposed to 24 h of ischemia and a subsequent 24 h of reperfusion. Analysis of mechanisms showed that hyperthermia could lead to a significant increase in HIF-1 alpha expression and also the HIF-1 binding activity in the ischemia/reperfusion astrocytes The data provide evidence to our hypothesis that the up-regulation of HIF-1 alpha is associated with the protective effects of hyperthermic preconditioning on astrocytes against ischemia/reperfusion injury (C) 2010 Elsevier B.V. All rights reserved
著者Du F, Zhu L, Qian ZM, Wu XM, Yung WH, Ke Y
期刊名稱BBA - Molecular Basis of Disease
詳細描述To ORKTS: doi: 10.1016/j.bbadis.2010.06.013
出版年份2010
月份11
日期1
卷號1802
期次11
出版社ELSEVIER SCIENCE BV
頁次1048 - 1053
國際標準期刊號0925-4439
電子國際標準期刊號0006-3002
語言英式英語
關鍵詞Apoptosis; Cell viability; Hyperthermiac preconditioning; Hypoxia-inducible factor-1 alpha (HIF-1 alpha); Ischemia/reperfusion; Lactate dehydrogenase (LDH); Reactive astrocytes
Web of Science 學科類別Biochemistry & Molecular Biology; BIOCHEMISTRY & MOLECULAR BIOLOGY; Biophysics; BIOPHYSICS; Cell Biology

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