Cerebral interleukin-6 is neuroprotective during permanent focal cerebral ischemia in the rat
Cerebral interleukin-6 is neuroprotective during permanent focal cerebral ischemia in the rat
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DOI：
10.1097/00004647-199802000-00008
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发表时间：
1998-02-01
影响因子：
6.3
通讯作者：
Rothwell, NJ
中科院分区：
文献类型：
--
作者：
Loddick, SA;Turnbull, AV;Rothwell, NJ
白细胞介素 - 6（IL - 6）是一种在神经元和神经胶质细胞中均有表达的神经营养细胞因子。本研究表明，大脑中动脉（MCAO）永久性闭塞所导致的脑缺血在MCAO后2小时内会使缺血半球的IL - 6生物活性显著增加（167 ± 55国际单位，而假手术组为：50 ± 35国际单位），并在8小时（3456 ± 1162国际单位）和24小时（6008 ± 1772国际单位）进一步增加。在另一系列实验中，脑室内注射重组IL - 6（3100或31000国际单位）在MCAO后显著减轻了缺血性脑损伤（分别为对照组的52%和65%）。内源性IL - 6生物活性在缺血时的大幅增加，以及外源性IL - 6产生的显著神经保护作用表明，这种细胞因子是脑缺血期间神经元死亡的一种重要内源性抑制剂。
Interleukin-6 (IL-6) is a neurotrophic cytokine expressed in both neurons and glia. The present study shows that cerebral ischemia produced by permanent occlusion of the middle cerebral artery (MCAO) produces a dramatic increase in IL-6 bioactivity in the ischemic hemisphere within 2 hours of MCAO (167 +/- 55 IU versus sham: 50 +/- 35 IU), with further increases at 8 hours (3,456 +/- 1,162 IU) and 24 hours (6,008 +/- 1,772 IU), In a separate series of experiments. intracerebroventricular injection of recombinant IL-6 (3,100 or 31,000 IU) significantly reduced ischemic brain damage Lifter MCAO (to 52% and 65% of controls, respectively). The large increase in endogenous IL-6 bioactivity in response to ischemia, together with the marked neuroprotection produced by exogenous IL-6 suggest that this cytokine is an important endogenous inhibitor of neuronal death during cerebral ischemia.