Suppr超能文献

有机碲化合物三氯(二氧乙烯-0,0')碲酸铵可提高小鼠缺血性中风模型中的神经元存活率并改善功能结局。

The organotellurium compound ammonium trichloro(dioxoethylene-0,0') tellurate enhances neuronal survival and improves functional outcome in an ischemic stroke model in mice.

作者信息

Okun Eitan, Arumugam Thiruma V, Tang Sung-Chun, Gleichmann Marc, Albeck Michael, Sredni Benjamin, Mattson Mark P

机构信息

CAIR Institute, Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.

出版信息

J Neurochem. 2007 Aug;102(4):1232-41. doi: 10.1111/j.1471-4159.2007.04615.x. Epub 2007 Apr 30.

Abstract

Ammonium trichloro(dioxoethylene-0,0') tellurate (AS101) is a non-toxic organotellurium compound with pleiotropic activities. It was recently shown to induce production of the neurotrophic factor glial cell line-derived neurotrophic factor and to rescue neuronal-like PC-12 cells from neurotrophic factor deprivation-induced apoptosis. In this study, we show that AS101 improves functional outcome and reduces brain damage in a mouse model of focal ischemic stroke. Both pre-stroke and post-stroke intraperitoneal treatments with AS101 reduced infarct size and edema and improved the neurological function of the animals. AS101 treatments reduced both apoptotic and inflammatory caspase activities, and also inhibited protein tyrosine nitration suggesting that AS101 suppresses oxidative stress. Studies of cultured neurons showed that AS101 confers protection against apoptosis induced by either glucose deprivation or the lipid peroxidation product 4-hydroxynonenal. Moreover, AS101 treatment reduced glutamate-induced intracellular calcium elevation, a major contributor to neuronal death in stroke. As AS101 has an excellent safety profile in humans, our pre-clinical data suggest a potential therapeutic benefit of AS101 in patients suffering from stroke and other neurodegenerative conditions.

摘要

三氯(二氧乙烯-0,0')碲酸铵(AS101)是一种具有多种活性的无毒有机碲化合物。最近的研究表明,它能诱导神经营养因子胶质细胞源性神经营养因子的产生,并使神经元样PC-12细胞免受神经营养因子剥夺诱导的凋亡。在本研究中,我们发现AS101在局灶性缺血性中风小鼠模型中可改善功能结局并减少脑损伤。中风前和中风后腹腔注射AS101均可减小梗死灶大小和减轻水肿,并改善动物的神经功能。AS101治疗降低了凋亡和炎性半胱天冬酶的活性,还抑制了蛋白质酪氨酸硝化,表明AS101可抑制氧化应激。对培养神经元的研究表明,AS101可保护细胞免受葡萄糖剥夺或脂质过氧化产物4-羟基壬烯醛诱导的凋亡。此外,AS101治疗可降低谷氨酸诱导的细胞内钙升高,而钙升高是中风时神经元死亡的主要原因。由于AS101在人体中具有良好的安全性,我们的临床前数据表明AS101对中风和其他神经退行性疾病患者具有潜在的治疗益处。

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