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大鼠实验性蛛网膜下腔出血后大脑动脉中 CD137 的表达:一项初步研究。

Expression of CD137 in the cerebral artery after experimental subarachnoid hemorrhage in rats: a pilot study.

机构信息

Department of Neurosurgery, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou 215006, Jiangsu Province, PR China.

出版信息

Brain Res. 2011 Apr 22;1386:200-8. doi: 10.1016/j.brainres.2011.02.049. Epub 2011 Feb 23.

DOI:10.1016/j.brainres.2011.02.049
PMID:21352817
Abstract

Inflammation and immunity play a crucial role in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). CD137 is recognized as an independent costimulatory molecule of T cells and activator of monocytes. A growing body of evidence indicates that CD137 is vital for inflammation and immunity. Therefore, this study aimed to investigate the expression of CD137 in the basilar artery in a rat SAH model and to clarify the potential role of CD137 in cerebral vasospasm. A total of 107 rats were randomly divided into four groups: control group; day 3, day 5, and day 7 groups. Day 3, day 5, and day 7 groups were all SAH groups. The animals in SAH groups were subjected to injection of autologous blood into cisterna magna twice on day 0 and day 2 and were sacrificed on days 3, 5, and 7, respectively. Cross-sectional area of basilar artery was measured and the CD137 expression was assessed by quantitative real-time PCR, Western blot and immunohistochemistry. The cross-sectional area of basilar artery was found to be 57,944±5581μm(2) in control group, 26,100±2639μm(2) in day 3, 19,723±2412μm(2) in day 5, and 28,800±2980μm(2) in day 7 group, respectively. The basilar artery exhibited vasospasm after SAH and became more severe on day 5. The elevated mRNA and protein of CD137 were detected after SAH and peaked on day 5. CD137 is increasingly expressed in a parallel time course to the development of cerebral vasospasm in a rat experimental model of SAH. These findings indicate the possible role of CD137 in the pathogenesis of cerebral vasospasm after SAH.

摘要

炎症和免疫在蛛网膜下腔出血(SAH)后脑血管痉挛的发病机制中起着至关重要的作用。CD137 被认为是 T 细胞的独立共刺激分子和单核细胞的激活剂。越来越多的证据表明,CD137 对炎症和免疫至关重要。因此,本研究旨在探讨 CD137 在大鼠 SAH 模型基底动脉中的表达情况,并阐明 CD137 在脑血管痉挛中的潜在作用。将 107 只大鼠随机分为四组:对照组;第 3 天、第 5 天和第 7 天组。第 3 天、第 5 天和第 7 天组均为 SAH 组。SAH 组动物于 0 天和 2 天两次向枕大池内注射自体血,分别于第 3、5 和 7 天处死。测量基底动脉横截面积,采用实时定量 PCR、Western blot 和免疫组织化学法检测 CD137 表达。对照组基底动脉横截面积为 57944±5581μm(2),第 3 天组为 26100±2639μm(2),第 5 天组为 19723±2412μm(2),第 7 天组为 28800±2980μm(2)。SAH 后基底动脉发生痉挛,第 5 天痉挛程度加重。SAH 后 CD137 的 mRNA 和蛋白表达升高,第 5 天达到高峰。CD137 在大鼠实验性 SAH 模型中,其表达与脑血管痉挛的发展呈平行时间过程,呈递增趋势。这些发现表明 CD137 可能在 SAH 后脑血管痉挛的发病机制中起作用。

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