首页> 外文期刊>American Journal of Physiology >Cerebellar stimulation reduces inducible nitric oxide synthase expression and protects brain from ischemia.
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Cerebellar stimulation reduces inducible nitric oxide synthase expression and protects brain from ischemia.

机译:小脑刺激降低了诱导型一氧化氮合酶的表达,并保护了大脑免于局部缺血。

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摘要

A focal infarction produced by occlusion of the middle cerebral artery (MCAO) in spontaneously hypertensive rats induced expression of inducible nitric oxide synthase (iNOS) mRNA, measured by competitive reverse transcription-polymerase chain reaction. The mRNA appeared simultaneously in the ischemic core and penumbra at 8 h, peaked between 14 and 24 h, and disappeared by 48 h. At 24 h, inducible nitric oxide synthase (iNOS)-like immunoreactivity was present in the endothelium of cerebral microvessels and in scattered cells, probably representing leukocytes or activated microglia. Electrical stimulation of the cerebellar fastigial nucleus (FN) for 1 h, 48 h before MCAO, reduced infarct volumes by 45% by decreasing cellular death in the ischemic penumbra. It also reduced by >90% the expression of iNOS mRNA and protein in the penumbra, but not core, and decreased by 44% the iNOS enzyme activity. We conclude that excitation of neuronal networks represented in the cerebellum elicits a conditioned central neurogenic neuroprotection associated with the downregulation of iNOS mRNA and protein. This neuroimmune interaction may, by blocking the expression of iNOS, contribute to neuroprotection.
机译:通过竞争性逆转录聚合酶链反应测量,自发性高血压大鼠大脑中动脉(MCAO)闭塞产生的局灶性梗死诱导了诱导型一氧化氮合酶(iNOS)mRNA的表达。 8小时时,mRNA同时出现在缺血核心和半影中,在14至24小时之间达到峰值,并在48小时时消失。在24小时时,脑微血管内皮和散在的细胞中存在诱导型一氧化氮合酶(iNOS)样的免疫反应,可能代表白细胞或活化的小胶质细胞。在MCAO之前48小时,电刺激小脑小脑顶核(FN)1小时,通过减少缺血半影中的细胞死亡,将梗死体积减少了45%。它还使半影中的iNOS mRNA和蛋白质表达减少了90%以上,但没有减少,而iNOS酶的活性减少了44%。我们得出结论,以小脑为代表的神经元网络的兴奋引发与iNOS mRNA和蛋白质下调相关的条件性中枢神经源性神经保护。这种神经免疫相互作用可以通过阻止iNOS的表达来促进神经保护。

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