Regulation of body temperature and neuroprotection by endogenous interleukin-6 in cerebral ischemia
Regulation of body temperature and neuroprotection by endogenous interleukin-6 in cerebral ischemia
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DOI：
10.1097/01.wcb.0000055177.50448.fa
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发表时间：
2003-04-01
影响因子：
6.3
通讯作者：
Schwaninger, M
中科院分区：
文献类型：
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作者：
Herrmann, O;Tarabin, V;Schwaninger, M
虽然发烧的功能还不清楚，但体温影响脑损伤的结果现在是毫无疑问的。体温升高通常见于中风患者，预示预后不良。然而，脑卒中后体温升高的病理生理基础和治疗方案仍不清楚。脑缺血可迅速诱导小鼠神经元白细胞介素-6（IL-6）表达。在IL-6缺陷小鼠中，大脑中动脉闭塞（MCAO）后体温显著降低，但梗死面积与对照小鼠相当。如果MCAO后通过外部加热控制体温，IL-6缺陷小鼠的存活率降低，神经系统状态更差，梗死面积比对照组更大。在细胞培养中，IL-6发挥抗凋亡和神经保护作用。这些数据表明，IL-6是体温的关键调节剂和脑缺血中的内源性神经保护剂。神经保护特性明显弥补了MCAO后的发热作用，并增强了这种内源性热原的安全性。
Although the function of fever is still unclear, it is now beyond doubt that body temperature influences the outcome of brain damage. An elevated body temperature is often found in stroke patients and denotes a bad prognosis. However, the pathophysiologic basis and treatment options of elevated body temperature after stroke are still unknown. Cerebral ischemia rapidly induced neuronal interleukin-6 (IL-6) expression in mice. In IL-6-deficient mice, body temperature was markedly decreased after middle cerebral artery occlusion (MCAO), but infarct size was comparable to that in control mice. If body temperature was controlled by external warming after MCAO, IL-6-deficient mice had a reduced survival, worse neurologic status, and larger infarcts than control animals. In cell culture, IL-6 exerted an antiapoptotic and neuroprotective effect. These data suggest that IL-6 is a key regulator of body temperature and an endogenous neuroprotectant in cerebral ischemia. Neuroprotective properties apparently compensate for its pyretic action after MCAO and enhance the safety of this endogenous pyrogen.