Inflammation and NFkappaB activation is decreased by hypothermia following global cerebral ischemia.
Inflammation and NFkappaB activation is decreased by hypothermia following global cerebral ischemia.
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DOI：
10.1016/j.nbd.2008.11.001
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发表时间：
2009-02
影响因子：
6.1
通讯作者：
Yenari MA
中科院分区：
文献类型：
--
作者：
Webster CM;Kelly S;Koike MA;Chock VY;Giffard RG;Yenari MA
我们之前的研究表明，低温通过抑制核因子κB （NFκB）的活化激酶来减轻局灶性脑缺血（FCI）的炎症。在这里，我们描述了全脑缺血（GCI）的炎症反应，以及亚低温的影响。通过双侧颈动脉闭塞对啮齿动物进行GCI。炎症反应伴有小胶质细胞激活，但不伴有中性粒细胞浸润或血脑屏障破坏。亚低温降低了CA1损伤，降低了小胶质细胞的激活，降低了核NFκB的易位和激活。在不引起脑细胞死亡的纯脑炎症模型中观察到类似的低体温抗炎作用。在低温条件下，缺氧葡萄糖剥夺（OGD）或LPS刺激的原代小胶质细胞的激活和NFκB易位也较少。然而，NFκB调节蛋白不受低温的影响。GCI后的炎症反应和低温的抗炎机制与FCI观察到的不同。
We previously showed that hypothermia attenuates inflammation in focal cerebral ischemia (FCI) by suppressing activating kinases of nuclear factor-kappa B (NFκB). Here we characterize the inflammatory response in global cerebral ischemia (GCI), and the influence of mild hypothermia. Rodents were subjected to GCI by bilateral carotid artery occlusion. The inflammatory response was accompanied by microglial activation, but not neutrophil infiltration, or blood brain barrier disruption. Mild hypothermia reduced CA1 damage, decreased microglial activation and decreased nuclear NFκB translocation and activation. Similar anti-inflammatory effects of hypothermia were observed in a model of pure brain inflammation that does not cause brain cell death. Primary microglial cultures subjected to oxygen glucose deprivation (OGD) or stimulated with LPS under hypothermic conditions also experienced less activation and less NFκB translocation. However, NFκB regulatory proteins were not affected by hypothermia. The inflammatory response following GCI and hypothermia’s anti-inflammatory mechanism is different from that observed in FCI.
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