Baicalein is neuroprotective in rat MCAO model: Role of 12/15-lipoxygenase, mitogen-activated protein kinase and cytosolic phospholipase A2
Baicalein is neuroprotective in rat MCAO model: Role of 12/15-lipoxygenase, mitogen-activated protein kinase and cytosolic phospholipase A2
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DOI：
10.1016/j.pbb.2010.07.007
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发表时间：
2010-10-01
影响因子：
3.6
通讯作者：
Du, Wei
中科院分区：
文献类型：
--
作者：
Cui, Lili;Zhang, Xiangjian;Du, Wei
炎症损伤和氧化应激在脑缺血发病机制中发挥重要作用，可能是治疗的目标。黄芩素是从传统中草药黄芩中分离出来的，一方面是抗氧化剂和抗炎剂，另一方面是脂氧合酶抑制剂。然而，关于黄芩素对缺血性中风的神经保护作用机制知之甚少。因此，我们研究了黄芩素的潜在神经保护作用并探讨了其潜在机制。对雄性Sprague-Dawley大鼠进行永久性大脑中动脉闭塞(MCAO)，并在脑缺血后立即静脉注射黄芩素。 MCAO 神经功能缺损后 24 小时，测量脑含水量和梗塞面积。采用免疫组织化学、蛋白质印迹和逆转录聚合酶链反应（RT-PCR）分析缺血脑皮质中12/15脂氧合酶（12/15-LOX）、p38丝裂原激活蛋白激酶（p38 MAPK）和胞质磷脂酶A2（cPIA2）基因和蛋白水平的表达。结果表明，黄芩素可改善神经功能缺损，减少脑含水量和梗塞面积，并下调 MCAO 中常见的 12/15-LOX、p38 MAPK 和 cPLA2 的过度表达。结果表明，黄芩素可以保护大脑免受MCAO造成的损伤，这种作用可能是通过下调12/15-LOX、p38 MAPK和cPLA2表达来实现的。 (C) 2010 Elsevier Inc. 保留所有权利。
Inflammatory damage and oxidative stress play an important role in cerebral ischemic pathogenesis and may represent a target for treatment. Baicalein, isolated from the traditional Chinese herbal medicine Huangqin, is an antioxidant and anti-inflammatory agent on one hand and a lipoxygenase inhibitor on the other hand. However, little is known regarding the mechanism of baicalein's neuroprotection in ischemic stroke. We therefore investigated the potential neuroprotective effects of baicalein and explored the underlying mechanisms. Male, Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (MCAO) and baicalein was administered intravenously immediately after cerebral ischemia. At 24 h after MCAO neurological deficit, brain water content and infarct sizes were measured. Immunohistochemistry, western blot and reverse transcription-polymerase chain reaction (RT-PCR) were used to analyse the expression of 12/15-lipoxygenase (12/15-LOX), p38 mitogen-activated protein kinase (p38 MAPK) and cytosolic phospholipase A2 (cPIA2) at gene and protein levels in ischemic brain cortex. The results showed that baicalein improved neurological deficit, reduced brain water content and infarct sizes, and downregulated the overexpression of 12/15-LOX, p38 MAPK and cPLA2 typically seen with MCAO. The results indicated that baicalein protected the brain from damage caused by MCAO, and this effect may be through downregulation of 12/15-LOX, p38 MAPK and cPLA2 expression. (C) 2010 Elsevier Inc. All rights reserved.