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3-硝基丙酸致大鼠脑代谢损伤后氧化还原调节蛋白硫氧还蛋白的表达与分布

Expression and distribution of redox regulatory protein, thioredoxin after metabolic impairment by 3-nitropropionic acid in rat brain.

作者信息

Sugino T, Nozaki K, Takagi Y, Hattori I, Hashimoto N, Yodoi J

机构信息

Department of Neurosurgery, Graduate School of Medicine, Kyoto University, Japan.

出版信息

Neurosci Lett. 1999 Nov 12;275(2):145-8. doi: 10.1016/s0304-3940(99)00763-6.

Abstract

Thioredoxin (TRX) is a small, multifunctional protein with a redox-active site and multiple biological functions that include reducing activity for reactive oxygen intermediates. We assayed TRX by immunohistochemical methods in the rat brain after intraperitoneal injection of 3-nitropropionic acid (3-NP), an irreversible inhibitor of succinate dehydrogenase. Systemic administration of 3-NP produced lateral striatal, hippocampal CA1 and CA3 lesions in the present study. The immunoreactivity for TRX was enhanced in hippocampal CA3, dentate gyrus and lateral striatum, but not detected in hippocampal CA1 subfield after 3-NP intoxication. The data suggest that TRX may play an important role in the pathogenesis of 3-NP neurotoxicity.

摘要

硫氧还蛋白(TRX)是一种小型多功能蛋白,具有氧化还原活性位点和多种生物学功能,包括对活性氧中间体的还原活性。我们采用免疫组化方法,在腹腔注射琥珀酸脱氢酶不可逆抑制剂3-硝基丙酸(3-NP)后的大鼠脑中检测TRX。在本研究中,全身给予3-NP会导致侧纹状体、海马CA1和CA3区出现损伤。3-NP中毒后,海马CA3区、齿状回和侧纹状体中TRX的免疫反应性增强,但在海马CA1亚区未检测到。数据表明,TRX可能在3-NP神经毒性的发病机制中起重要作用。

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