...
【24h】

Aggravated chronic brain injury after focal cerebral ischemia in aquaporin-4-deficient mice

机译:水通道蛋白4缺陷小鼠局灶性脑缺血后加重的慢性脑损伤

获取原文
获取原文并翻译 | 示例
           

摘要

The water channel aquaporin-4 (AQP4) is important in brain water homeostasis, and is also involved in astrocyte growth and glial scar formation. It has been reported that AQP4 deficiency attenuates acute ischemic brain injury as a result of reducing cytotoxic edema. Here, we determined whether AQP4 deficiency influences chronic brain injury after focal cerebral ischemia induced by 30min of middle cerebral artery occlusion (MCAO). AQP4 -/- mice exhibited a lower survival rate and less body weight gain than wild-type mice, but their neurological deficits were similar to wild-type mice during 35 days after MCAO. At 35 days after MCAO, AQP4 -/- mice showed more severe brain atrophy and cavity formation in the ischemic hemisphere as well as more neuronal loss in the hippocampus. Furthermore, astrocyte proliferation and glial scar formation were impaired in AQP4 -/- mice. Therefore, AQP4 deficiency complicated by astrocyte dysfunction aggravates chronic brain injury after focal cerebral ischemia, suggesting that AQP4 may be important in the chronic phase of the post-ischemic recovery process.
机译:水通道aquaporin-4(AQP4)在脑水稳态中很重要,并且还参与星形胶质细胞的生长和胶质瘢痕的形成。据报道,由于减少了细胞毒性水肿,AQP4缺乏减轻了急性缺血性脑损伤。在这里,我们确定AQP4缺乏是否影响由大脑中动脉闭塞(MCAO)30分钟引起的局灶性脑缺血后的慢性脑损伤。 AQP4-/-小鼠比野生型小鼠表现出更低的存活率和更少的体重增加,但是在MCAO后的35天内,它们的神经功能缺损与野生型小鼠相似。 MCAO后35天,AQP4-/-小鼠在缺血性半球表现出更严重的脑萎缩和空腔形成,在海马区表现出更多的神经元丢失。此外,在AQP4-/-小鼠中星形胶质细胞增殖和胶质瘢痕形成受到损害。因此,AQP4缺乏症并发星形胶质细胞功能障碍会加重局灶性脑缺血后的慢性脑损伤,这表明AQP4在缺血后恢复过程的慢性阶段可能很重要。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号