Expression and cell distribution of leukotriene B4 receptor 1 in the rat brain cortex after experimental subarachnoid hemorrhage.
Expression and cell distribution of leukotriene B4 receptor 1 in the rat brain cortex after experimental subarachnoid hemorrhage.
复制标题
实验性蛛网膜下腔出血后大鼠脑皮质白三烯B4受体1的表达及细胞分布
DOI：
10.1016/j.brainres.2016.10.006
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发表时间：
2016
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：
Ye Zhen-Nan;Zhuang Zong;Wu Ling-Yun;Liu Jing-Peng;Chen Qiang;Zhang Xiang-Sheng;Zhou Meng-Liang;Zhang Zi-Huan;Li Wei;Wang Xiao-Liang;Hang Chun-Hua
Convincing evidence supports that nuclear factor kappa B (NF-κB)-meditated inflammation contributes to the adverse prognosis of aneurysmal subarachnoid hemorrhage (SAH), and pathologic neutrophil accumulation after SAH in the brain parenchyma enhances the inflammatory process. Leukotriene B4 (LTB4) is a highly potent lipid chemoattractant of neutrophils, and its biological effects are mediated primarily through the high-affinity LTB4 receptor 1 (BLT1). It is verified that NF-κB-dependent BLT1 mediates LTB4 signaling and LTB4 stimulates NF-κB-dependent inflammation via BLT1. This study aimed to determine the expression and cell distribution of BLT1 in the brain cortex after SAH and investigate the potential relationship between protein expressions of BLT1 and NF-κB. Male Sprague-Dawley rats were randomly assigned into sham group and SAH groups at 6 h, 12 h and on day 1, day 2 and day 3 (n=6 for each subgroup). SAH groups suffered experimental SAH by injecting 0.3 ml autologous blood into the prechiasmatic cistern. BLT1 expression was measured by real-time PCR, western blot, immunohistochemistry and immunofluorescence. Nuclear expression of p65 protein, the major subunit of NF-κB, was also detected by western blot. Our data showed that the expression levels of BLT1 and nuclear p65 protein were both markedly increased after SAH. Moreover, there was a significant positive correlation between BLT1 and nuclear p65 protein expressions in the same specific time course. Double immunofluorescence staining showed that BLT1 were mainly expressed in neurons, microglia and endothelial cells rather than astrocytes after SAH. These results suggest that BLT1 may participate in the NF-κB-mediated inflammatory response after SAH, and there might be important implications for further studies using specific BLT1 antagonists to attenuate the NF-κB-mediated inflammation after SAH.
