Suppr超能文献

年龄调节缺血性小脑一氧化氮系统的反应。

Age modulates the nitric oxide system response in the ischemic cerebellum.

作者信息

Blanco Santos, Castro Lourdes, Hernández Raquel, Del Moral María Luisa, Pedrosa Juan Angel, Martínez-Lara Esther, Siles Eva, Peinado María Angeles

机构信息

Department of Experimental Biology, University of Jaén, Paraje Las Lagunillas s/n, 23071, Jaén, Spain.

出版信息

Brain Res. 2007 Jul 9;1157:66-73. doi: 10.1016/j.brainres.2007.01.141. Epub 2007 Feb 17.

Abstract

To determine whether age influences the nitric oxide system response to ischemia in the cerebellum, we have analyzed the levels of nitrogen oxides (NOx) and the expression of the different nitric oxide synthase isoforms (NOS) in mature adult (4-5 months old) and aged rats (24-27 months old) subjected to a transient global ischemia/reperfusion (I/R) model. We also analyzed the nitrated proteins and the glial fibrillary acidic protein (GFAP) expression. NOx concentration in adult rats, which more than doubled the values found in the aged rats, decreased after the ischemia and reperfusion. However, in the aged animals, these NOx levels did not significantly change after I/R. Constitutive isoforms were first down-regulated in the ischemic period, in both adult and aged animals. However, after 6 h of reperfusion, these isoforms were up-regulated, but only in aged rats. After I/R, iNOS was up-regulated in adults but down-regulated in the aged rats. Hence, after an episode of transient global ischemia and reperfusion, the aged cerebellum maintains a balanced NO production, silencing the iNOS isoform and inducing a weak expression of nNOS and eNOS; this allows NO physiological functions while avoiding possible undesirable effects such as the nitrative damage or astrocyte activation.

摘要

为了确定年龄是否会影响小脑对缺血的一氧化氮系统反应,我们分析了成熟成年大鼠(4 - 5个月大)和老年大鼠(24 - 27个月大)在经历短暂性全脑缺血/再灌注(I/R)模型后氮氧化物(NOx)的水平以及不同一氧化氮合酶同工型(NOS)的表达。我们还分析了硝化蛋白和胶质纤维酸性蛋白(GFAP)的表达。成年大鼠的NOx浓度在缺血和再灌注后降低,其值比老年大鼠高出一倍多。然而,在老年动物中,I/R后这些NOx水平没有显著变化。组成型同工型在成年和老年动物的缺血期均首先下调。然而,再灌注6小时后,这些同工型上调,但仅在老年大鼠中出现。I/R后,诱导型一氧化氮合酶(iNOS)在成年大鼠中上调,而在老年大鼠中下调。因此,在经历短暂性全脑缺血和再灌注后,老年小脑维持一氧化氮的平衡产生,使iNOS同工型沉默,并诱导神经元型一氧化氮合酶(nNOS)和内皮型一氧化氮合酶(eNOS)的弱表达;这既能实现一氧化氮的生理功能,又能避免可能出现的不良影响,如硝化损伤或星形胶质细胞激活。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验