首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >A possible role of endogenous central corticotrophin releasing factor in lipopolysaccharide induced thymic involution and cell apoptosis: Effect of peripheral injection of corticotrophin releasing factor
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A possible role of endogenous central corticotrophin releasing factor in lipopolysaccharide induced thymic involution and cell apoptosis: Effect of peripheral injection of corticotrophin releasing factor

机译:内源性促肾上腺皮质激素释放因子在脂多糖诱导的胸腺复性和细胞凋亡中的可能作用:外周注射促肾上腺皮质激素释放因子的作用

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摘要

The aim of the study was to investigate the role of endogenous peripheral and central corticotrophin-releasing factor (CRF) following lipopolysaccharide (LPS) challenge on thymic involution and apoptosis. Administration of LPS (100 mu g/mouse, ip) led to thymic involution, to a decrease of CD4 + CD8 + thymocyte subset, and to fragmentation of thymic DNA Pretreatment of LPS challenged mice with intracerebroventricular a-helical CRF (a CRF antagonist) attenuated the effect of LPS however, intraventricular administered alpha-helical CRF failed to affect LPS response on thymus. Moreover, the effects of LPS on thymus, examined on 1,7 and 14 days were wholly abrogated by prior administration of intraventricular CRF (10 mu g/animal). The plasma corticosterone levels were found to be decreased with single dose of peripheral CRF in LPS challenged mice. These findings indicate that central endogenous CRF involved in LPS induced thymic atrophy. However, peripheral CRF offers protective effect on LPS induced thymic involution and cell apoptosis. (C) 2015 Elsevier B.V. All rights reserved.
机译:这项研究的目的是调查脂多糖(LPS)攻击后内源性外周和中央促肾上腺皮质激素释放因子(CRF)对胸腺复性和细胞凋亡的作用。给予LPS(100μg /小鼠,腹膜内)导致胸腺退化,减少CD4 + CD8 +胸腺细胞亚群,并导致胸腺DNA断裂用脑室内a螺旋CRF(一种CRF拮抗剂)预处理LPS攻击的小鼠减弱了LPS的作用,但是,脑室内给予的α-螺旋CRF不能影响LPS对胸腺的反应。此外,在事先服用脑室内CRF(10μg/动物)后,在第1、7和14天检查的LPS对胸腺的影响被完全消除。发现在受LPS攻击的小鼠中,血浆皮质酮水平随单剂量外周CRF降低。这些发现表明,参与LPS的中央内源性CRF引起胸腺萎缩。然而,外周CRF对LPS诱导的胸腺退化和细胞凋亡提供保护作用。 (C)2015 Elsevier B.V.保留所有权利。

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