Inhibition of leukotriene B4 synthesis protects against early brain injury possibly via reducing the neutrophil-generated inflammatory response and oxidative stress after subarachnoid hemorrhage in rats.
Inhibition of leukotriene B4 synthesis protects against early brain injury possibly via reducing the neutrophil-generated inflammatory response and oxidative stress after subarachnoid hemorrhage in rats.
复制标题
抑制白三烯 B4 合成可能通过减少大鼠蛛网膜下腔出血后中性粒细胞产生的炎症反应和氧化应激来预防早期脑损伤
DOI：
10.1016/j.bbr.2017.11.011
复制
发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Hang Chun-Hua
中科院分区：
文献类型：
--
作者：
Ye Zhen-Nan;Wu Ling-Yun;Liu Jing-Peng;Chen Qiang;Zhang Xiang-Sheng;Lu Yue;Zhou Meng-Liang;Li Wei;Zhang Zi-Huan;Xia Da-Yong;Zhuang Zong;Hang Chun-Hua
白三烯B4（LTB 4）是一种高效的中性粒细胞化学引诱物，当中性粒细胞募集并浸润到损伤/炎症部位（例如蛛网膜下腔出血（SAH）后的脑实质）时，它们诱导炎症反应和氧化应激。本研究旨在探讨抑制LTB 4合成对SAH后中性粒细胞募集、炎症反应和氧化应激以及早期脑损伤（EBI）的影响。本实验采用大鼠视交叉池前SAH模型。SC 57461 A通过脑室内注射用于抑制LTB 4合成。对SAH后颞叶脑组织进行分析。通过观察脑水肿、神经元损伤及神经功能恢复情况，了解EBI的发生发展过程。我们发现抑制SAH后LTB 4的合成可以降低SAH后24 h的髓过氧化物酶水平，减轻炎症反应和氧化应激，减少脑实质中神经元的死亡，改善脑水肿和神经行为障碍。这些结果表明，抑制LTB 4的合成可能会减轻EBI后SAH可能通过减少嗜中性粒细胞产生的炎症反应和氧化应激。
Leukotriene B4 (LTB4) is a highly potent neutrophil chemoattractant and neutrophils induces inflammatory response and oxidative stress when they recruit to and infiltrate in the injuried/inflamed site, such as the brain parenchyma after aneurysmal subarachnoid hemorrhage (SAH). This study is to investigate the potential effects of inhibition of LTB4 synthesis on neutrophil recruitment, inflammatory response and oxidative stress, as well as early brain injury (EBI) in rats after SAH. A pre-chiasmatic cistern SAH model of rats was used in this experiment. SC 57461A was used to inhibit LTB4 synthesis via intracerebroventricular injection. The brain tissues of temporal lobe after SAH were analyzed. Neuronal injury, brain edema and neurological function were evaluated to investigate the development of EBI. We found that inhibition of LTB4 synthesis after SAH could reduce the level of myeloperoxidase, alleviate the inflammatory response and oxidative stress, and reduce neuronal death in the brain parenchyma, and ameliorate brain edema and neurological behavior impairment at 24 h after SAH. These results suggest that inhibition of LTB4 synthesis might alleviate EBI after SAH possibly via reducing the neutrophil-generated inflammatory response and oxidative stress.