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后适应有效地预防三甲基锡诱导的大鼠脑神经元损伤。

Postconditioning Effectively Prevents Trimethyltin Induced Neuronal Damage in the Rat Brain.

作者信息

Lalkovicova Maria, Burda Jozef, Nemethova Miroslava, Burda Rastislav, Danielisova Viera

出版信息

Folia Biol (Krakow). 2016;64(2):97-103. doi: 10.3409/fb64_2.97.

DOI:10.3409/fb64_2.97
PMID:29537191
Abstract

Trimethyltin (TMT) is a toxic substance formerly used as a catalyst in the production of organic substances, as well as in industry and agriculture. TMT poisoning has caused death or severe injury in many dozens of people. The toxicity of TMT is mediated by dose dependent selective damage to the limbic system in humans and other animals, specifically the degeneration of CA1 neurons in the hippocampus. The typical symptoms include memory loss and decreased learning ability. Using knowledge gained in previous studies of global ischaemia, we used delayed postconditioning after TMT intoxication (8 mg/kg i.p.), consisting of applying a stressor (BR, bradykinin 150 μg/kg i.p.) 24 or 48 hours after the injection of TMT. We found that BR had preventive effects on neurodegenerative changes as well as learning and memory deficits induced by TMT intoxication.

摘要

三甲基锡(TMT)是一种有毒物质,以前在有机物质生产以及工农业中用作催化剂。TMT中毒已导致数十人死亡或重伤。TMT的毒性是通过对人类和其他动物边缘系统的剂量依赖性选择性损伤介导的,特别是海马体中CA1神经元的退化。典型症状包括记忆力减退和学习能力下降。利用先前在全脑缺血研究中获得的知识,我们在TMT中毒(腹腔注射8mg/kg)后采用延迟后处理,即在注射TMT后24或48小时施加应激源(缓激肽,腹腔注射150μg/kg)。我们发现缓激肽对TMT中毒引起的神经退行性变化以及学习和记忆缺陷具有预防作用。

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