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短暂性全脑缺血后硫酸化糖蛋白-2(聚集素)和胶质纤维酸性蛋白(GFAP)RNA表达的诱导被LY231617差异性减弱。

Induction of sulfated glycoprotein-2 (clusterin) and glial fibrillary acidic protein (GFAP) RNA expression following transient global ischemia is differentially attenuated by LY231617.

作者信息

May P C, Clemens J A, Panetta J A, Smalstig E B, Stephenson D, Fuson K S

机构信息

Lilly Research Laboratories, CNS Research, Eli Lilly and Company, Indianapolis, IN 46285, USA.

出版信息

Brain Res Mol Brain Res. 1996 Nov;42(1):145-8. doi: 10.1016/s0169-328x(96)00155-6.

Abstract

Sulfated glycoprotein-2 (SGP-2) is a secreted glycoprotein that along with GFAP has emerged as a prominent molecular marker of neurodegeneration. In the present study, we have evaluated further the relationship between SGP-2, GFAP and neurodegeneration, by examining the effects of LY231617, a potent antioxidant, on expression of SGP-2 and GFAP following four vessel occlusion (4VO). GFAP and SGP-2 RNA levels increased several fold in hippocampus and caudate nucleus in response to 30 min of 4VO. LY231617 treatment markedly attenuated the induction of GFAP RNA in both hippocampus and caudate nucleus, consistent with the significant neuroprotection observed histologically. In contrast, LY231617 treatment blunted SGP-2 RNA expression only in the hippocampus; SGP-2 RNA expression in caudate nucleus was similar to vehicle-treated 4VO, despite the marked attenuation of neuronal damage in both areas by LY231617. These data suggest region-specific differential regulation of SGP-2 and GFAP RNA induction.

摘要

硫酸化糖蛋白-2(SGP-2)是一种分泌型糖蛋白,它与胶质纤维酸性蛋白(GFAP)一起,已成为神经退行性变的重要分子标志物。在本研究中,我们通过检测强效抗氧化剂LY231617对四血管闭塞(4VO)后SGP-2和GFAP表达的影响,进一步评估了SGP-2、GFAP与神经退行性变之间的关系。在4VO持续30分钟后,海马体和尾状核中的GFAP和SGP-2 RNA水平增加了几倍。LY231617治疗显著减弱了海马体和尾状核中GFAP RNA的诱导,这与组织学观察到的显著神经保护作用一致。相比之下,LY231617治疗仅使海马体中的SGP-2 RNA表达减弱;尽管LY231617显著减轻了两个区域的神经元损伤,但尾状核中的SGP-2 RNA表达与用载体处理的4VO相似。这些数据表明SGP-2和GFAP RNA诱导存在区域特异性差异调节。

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