Expression and cell distribution of myeloid differentiation primary response protein 88 in the cerebral cortex following experimental subarachnoid hemorrhage in rats: A pilot study
Expression and cell distribution of myeloid differentiation primary response protein 88 in the cerebral cortex following experimental subarachnoid hemorrhage in rats: A pilot study
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大鼠实验性蛛网膜下腔出血后大脑皮质中骨髓分化初级反应蛋白 88 的表达和细胞分布：一项初步研究
DOI：
10.1016/j.brainres.2013.05.010
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发表时间：
2013-07-03
期刊：
影响因子：
2.9
通讯作者：
Hang, Chun-hua
中科院分区：
文献类型：
--
作者：
Sun, Qing;Dai, Yuxiang;Hang, Chun-hua
蛛网膜下腔出血（Subarachnoid hemorrhage，SAH）主要由动脉瘤破裂引起，每年造成大量死亡。令人信服的证据表明，炎症有助于SAH引起的不良结局。Toll样受体（TLR）、核因子-κ B（NF-κ B）、白细胞介素1 β（IL-1 β）和肿瘤坏死因子-α（TNF-α）参与SAH后的损伤性炎症过程。髓样分化初级应答蛋白88（MyD 88）对于将TLR信号传递至NF-κ B和促炎因子是必需的。本研究旨在检测MyD 88在SAH中的表达水平，进一步了解MyD 88在SAH中的作用。SD大鼠随机分为假手术组和SAH 2 h、6 h、12 h组，SAH 1、2、3、5、7 d组。蛛网膜下腔出血组（SAH组）于视交叉前池注入自体血0.3ml，造成实验性蛛网膜下腔出血。MyD 88表达通过蛋白质印迹分析、实时聚合酶链反应（PCR）、免疫组织化学和免疫荧光测量。通过实时PCR测量TNF-α和IL-1 β的水平。结果表明，MyD 88在SAH后表达增强，在第1天和第5天达到高峰，与IL-1 β的上调呈平行的时间过程，二者之间呈高度正相关。免疫组化和免疫荧光结果显示，MyD 88主要在神经元中表达，在星形胶质细胞和小胶质细胞中也有过表达。这些结果可能具有重要的意义，在特定的MyD 88拮抗剂的管理，以防止或减少SAH后的炎症反应。(c)2013爱思唯尔有限公司版权所有。
Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that inflammation contributes to the poor outcome caused by SAH. Toll like receptors (TLRs), nuclear factor-kappaB (NF-kappa B), Interleukin 1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) are involved in the damaging inflammation process after SAH. Myeloid differentiation primary response protein 88 (MyD88) is essential to deliver TLRs signals down to NF-kappa B and pro-inflammatory factors. The study aims to detect the expression level of MyD88 and know more about the role of MyD88 after SAH. Sprague Dawley (SD) rats were randomly divided into sham group and SAH groups at 2 h, 6 h, 12 h and on day 1, day 2, day 3, day 5 and day 7. SAH groups suffered experimental subarachnoid hemorrhage by injection of 0.3 ml autoblood into the pre-chiasmatic cistern. MyD88 expression is measured by western blot analysis, real-time polymerase chain reaction (PCR), immunohistochemistry and immunofluorescence. The levels of TNF-alpha and IL-1 beta were measured by real-time PCR. Our results demonstrated MyD88 expression was increased after SAH, and peaked on day 1 and day 5, which showed a parallel time course to the up-regulation of IL-1 beta, there was a highly positive relationship between them. Immunohistochemistry and immunofluorescence results indicated up-regulated MyD88 was mainly located in neurons while over expressed MyD88 could also be found in astrocytes and microglia. These results might have important implications during the administration of specific MyD88 antagonists in order to prevent or reduce inflammatory response following SAH. (c) 2013 Elsevier B.V. All rights reserved.