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首页> 外文期刊>Translational Stroke Research >Role of the Sphingosine Metabolism Pathway on Neurons Against Experimental Cerebral Ischemia in Rats
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Role of the Sphingosine Metabolism Pathway on Neurons Against Experimental Cerebral Ischemia in Rats

机译：鞘氨醇代谢途径在神经元中对大鼠实验性脑缺血的作用

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Although there is evidence that sphingosine-1-phosphate receptor-1 (S1P1) activation occurs following experimental brain injury, there is little information about its metabolic pathway in cerebral ischemia. The purpose of this study was to evaluate the role of the sphingosine metabolic pathway including S1P1 and sphingosine kinases 1 (SphK1) and 2 (SphK2) in transient middle cerebral artery occlusion (MCAO). Fifty-eight male Sprague–Dawley rats were used to assess temporal profiles of S1P1, SphK1, and SphK2 on neurons in infarct and periinfarct cortices at preinfarct state, 6 h, and 24 h after MCAO. The animals were then treated with vehicle and 0.25 mg/kg FTY720, which is an agonist of S1P receptors, and evaluated regarding neurological function, infarct volume, and S1P1 expression on neurons at 24 h after MCAO. The expressions of S1P1, SphK1, and SphK2 were significantly decreased after MCAO. Labeling of all markers was reduced in the infarct cortex but remained present in the periinfarct cortex and some were found to be on neurons. Significant improvements of neurological function and brain injury were observed in the FTY720 group compared with the vehicle and untreated groups, although S1P1 expression on neurons was reduced in the FTY720 group compared with the vehicle group. We demonstrated that S1P1, SphK1, and SphK2 were downregulated in the infarct cortex, whereas they were preserved in the periinfarct cortex where FTY720 reduced neuronal injury possibly via S1P1 activation. Our findings suggest that activation of the sphingosine metabolic pathway may be neuroprotective in cerebral ischemia.
机译：尽管有证据表明神经鞘氨醇-1-磷酸受体-1（S1P1）激活在实验性脑损伤后发生，但关于其在脑缺血中的代谢途径的信息很少。这项研究的目的是评估包括S1P1和鞘氨醇激酶1（SphK1）和2（SphK2）在内的鞘氨醇代谢途径在短暂性大脑中动脉阻塞（MCAO）中的作用。 58只雄性Sprague-Dawley大鼠用于评估梗死前状态，MCAO后6小时和24小时，梗死和梗死周围皮层神经元的S1P1，SphK1和SphK2的时空分布。然后将动物用媒介物和0.25 mg / kg STYP受体激动剂FTY720治疗，并在MCAO后24小时评估其神经功能，梗塞体积和S1P1在神经元上的表达。 MCAO后，S1P1，SphK1和SphK2的表达明显降低。在梗塞皮层中所有标记物的标记减少，但仍存在于梗死皮层中，并且发现某些标记在神经元上。与载体和未治疗组相比，FTY720组观察到神经功能和脑损伤有显着改善，尽管与载体组相比，FTY720组神经元上的S1P1表达降低。我们证明了S1P1，SphK1和SphK2在梗死皮层中被下调，而它们保留在梗死皮层中，其中FTY720可能通过S1P1激活减轻了神经元损伤。我们的发现表明鞘氨醇代谢途径的激活可能在脑缺血中具有神经保护作用。

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