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Functional deterioration of endothelial nitric oxide synthase after focal cerebral ischemia

机译:局灶性脑缺血后内皮型一氧化氮合酶的功能退化

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摘要

Endothelial nitric oxide synthase (eNOS) dysfunction is related to secondary injury and lesion expansion after cerebral ischemia. To date, there are few reports about postischemic alterations in the eNOS regulatory system. The purpose of the present study was to clarify eNOS expression, Ser1177 phosphorylation, and monomer formation after cerebral ischemia. Male Wistar rats were subjected to transient focal cerebral ischemia. Endothelial nitric oxide synthase messenger RNA (mRNA) and protein expression increased ∼8-fold in the ischemic lesion. In the middle cerebral artery core, eNOS-Ser1177 phosphorylation increased 6 hours after ischemia; however, there was an approximately 90% decrease in eNOS-Ser1177 phosphorylation observed 24 hours after ischemia that continued until at least 7 days after ischemia. Endothelial nitric oxide synthase monomer formation also increased 24 and 48 hours after ischemia (P<0.05), and protein nitration progressed in parallel with monomerization. To assess the effect of a neuroprotective agent on eNOS dysfunction, we evaluated the effect of fasudil, a Rho-kinase inhibitor, on eNOS phosphorylation and dimerization. Postischemic treatment with fasudil suppressed lesion expansion and dephosphorylation and monomer formation of eNOS. In conclusion, functional deterioration of eNOS progressed after cerebral ischemia. Rho-kinase inhibitors can reduce ischemic lesion expansion as well as eNOS dysfunction in the ischemic brain.
机译:内皮型一氧化氮合酶(eNOS)功能障碍与脑缺血后继发性损伤和病变扩展有关。迄今为止,关于eNOS调节系统中缺血后改变的报道很少。本研究的目的是阐明脑缺血后eNOS的表达,Ser1177磷酸化和单体形成。雄性Wistar大鼠经历短暂性局灶性脑缺血。在缺血性病变中,内皮一氧化氮合酶信使RNA(mRNA)和蛋白质表达增加了约8倍。缺血后6小时,在大脑中动脉核心,eNOS-Ser1177的磷酸化增加。但是,缺血后24小时观察到的eNOS-Ser1177磷酸化水平下降了约90%,这种现象持续到缺血后至少7天。缺血后24和48小时,内皮一氧化氮合酶单体的形成也增加(P <0.05),并且蛋白质的硝化与单体化同时进行。为了评估神经保护剂对eNOS功能障碍的影响,我们评估了Rho激酶抑制剂法舒地尔对eNOS磷酸化和二聚化的影响。用法舒地尔进行缺血后治疗可抑制病灶扩展,去磷酸化和eNOS单体形成。总之,脑缺血后eNOS的功能恶化。 Rho激酶抑制剂可减少缺血性脑病的缺血性病变扩展以及eNOS功能障碍。

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