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首页> 外文学位 >Galantamine prevents soman-induced apoptotic cell death in the guinea pig brain.
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Galantamine prevents soman-induced apoptotic cell death in the guinea pig brain.

机译：加兰他敏可防止豚鼠脑中梭曼诱导的凋亡细胞死亡。

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摘要

Galantamine, a drug approved for treatment of Alzheimer's disease, prevents the acute toxicity and the neurodegeneration induced by organophosphorous poisons, including soman. The present study was designed to identify soman-induced neurotoxicity and its protection by galantamine. Male pre-pubertal guinea pigs were treated with: (i) saline (0.5 ml/kg, im), (ii) galantamine (8 mg/kg, im), (iii) 1xLD50 soman (28 microg/kg, sc), or (iv) galantamine 30 min before soman. All animals, except those challenged with soman alone, survived. Only 50% of the soman-challenged, untreated guinea pigs survived; about 75% of the survivors had mild or severe signs of intoxication and were studied herein. At 24 h after each treatment, animals were euthanized, and their brains removed for analysis of cell viability, enzyme activity, protein expression and neuronal death.;In histological studies, large numbers of neurons were stained with Fluoro Jade-B (FJ-B), a fluorescent marker of neurodegeneration, in the amygdala, piriform cortex, and cerebral cortex, but rarely in the hippocampus of soman-injected animals. TUNEL-positive cells were also visualized in different brain regions of soman-challenged guinea pigs. Caspase 3/7 activity was higher in the brains taken from animals 2h after their challenge with soman than in the brains of control animals. In the brains of soman-injected guinea pigs that were pre-treated with galantamine, there were no FJ-B-positive cells and no TUNEL-positive cells. In addition, caspase activity in the brain of soman-challenged guinea pigs that were treated with galantamine was comparable to control.;These results indicate that: (i) neurodegeneration induced by soman is in part a result of the activation of a caspase-dependent apoptotic pathway, and (ii) pre-treatment with galantamine can effectively prevent soman-induced neurodegeneration.
机译：加兰他敏（Galantamine）是一种被批准用于治疗阿尔茨海默氏病的药物，可防止由有机磷毒物（包括梭曼）引起的急性毒性和神经变性。本研究旨在确定梭曼诱导的神经毒性及其加兰他敏的保护作用。用（i）生理盐水（0.5 ml / kg，im），（ii）加兰他敏（8 mg / kg，im），（iii）1xLD50梭曼（28 microg / kg，sc）处理雄性青春期前豚鼠或（iv）梭曼前30分钟加兰他敏。除仅接受梭曼攻击的动物外，所有动物均存活。经梭曼攻击，未经治疗的豚鼠中只有50％存活；约75％的幸存者有轻度或严重中毒迹象，在此进行了研究。每次治疗后24小时，对动物实施安乐死，并切除大脑以分析细胞活力，酶活性，蛋白质表达和神经元死亡。在组织学研究中，大量的神经元被Fluoro Jade-B（FJ-B）染色），是杏仁体，梨状皮层和大脑皮层中神经变性的荧光标记，但在注射梭曼的动物的海马中很少见。在梭曼攻击的豚鼠的不同大脑区域中，还可以看到TUNEL阳性细胞。梭曼攻击后2h取自动物的大脑中的caspase 3/7活性高于对照动物的脑中。在用加兰他敏预处理的注射梭曼的豚鼠的大脑中，没有FJ-B阳性细胞，也没有TUNEL阳性细胞。此外，用加兰他敏治疗的梭曼攻击豚鼠的大脑中的半胱天冬酶活性与对照相当；这些结果表明：（i）梭曼诱导的神经变性部分是由于半胱氨酸天冬氨酸依赖的活化凋亡途径，以及（ii）加兰他敏预处理可以有效预防梭曼诱导的神经变性。

著录项

  • 作者

    Kulkarni, Girish S.;

  • 作者单位

    University of Maryland, Baltimore.;

  • 授予单位 University of Maryland, Baltimore.;
  • 学科 Biology Neuroscience.;Health Sciences Toxicology.
  • 学位 Ph.D.
  • 年度 2012
  • 页码 234 p.
  • 总页数 234
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 地球物理学;
  • 关键词

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