首页> 外文期刊>Brain research >Bradykinin preconditioning modulates aquaporin-4 expression after spinal cord ischemic injury in rats.
【24h】

Bradykinin preconditioning modulates aquaporin-4 expression after spinal cord ischemic injury in rats.

机译:缓激肽预处理可调节大鼠脊髓缺血损伤后水通道蛋白4的表达。

获取原文
获取原文并翻译 | 示例
           

摘要

The study investigated whether bradykinin (BK) preconditioning could regulate the expression of aquaporin-4 (AQP4) using an in vivo transient spinal cord ischemia model in rats. BK was infused continuously via the left femoral artery with infusion pump for 15 min (10 microg/kg/min) then we induced ischemia for 20 min and reperfusion for 24 and 72 h respectively. The results demonstrated that the central part of the white matter exhibited loss of perivascular AQP4 and showed a partial recovery toward 72 h of reperfusion. The border zone of white matter was different from the central part of the white matter by showing no loss of perivascular AQP4 at 24 h of reperfusion but rather a slight increase. BK significantly reduced the expression level of AQP4 protein in the white matter, but it had none of this effect in the gray matter region at 72 h post-reperfusion. There was no difference in AQP4 protein levels between BK group and control group at the two above-mentioned spinal cord regions at 24 h after reperfusion. In addition, the changes in AQP4 protein induced by BK preconditioning were obvious at 72 h after reperfusion, which were accompanied by a reduction of spinal cord edema. Our results demonstrated that the expression of AQP4 protein after spinal cord ischemia/reperfusion was region-specific, time-dependent and also indicated that the attenuation of AQP4 expression induced by BK could be one of the important molecular mechanisms in physiopathology of spinal cord ischemic edema.
机译:该研究使用大鼠体内短暂性脑缺血模型研究缓激肽(BK)预处理是否可以调节aquaporin-4(AQP4)的表达。用输注泵通过左股动脉连续注入BK 15分钟(10微克/千克/分钟),然后诱导缺血20分钟,再灌注分别24和72小时。结果表明,白质的中央部分表现出血管周AQP4的丧失,并在再灌注72 h时部分恢复。白质的边界区与白质的中心部分不同,在再灌注24 h时血管周围AQP4并未丢失,但略有增加。 BK显着降低了白质中AQP4蛋白的表达水平,但在再灌注后72 h,它在灰质区域中没有这种作用。再灌注后24小时,上述两个脊髓区域的BK组和对照组之间的AQP4蛋白水平没有差异。此外,BK预处理诱导的AQP4蛋白变化在再灌注后72 h明显,并伴有脊髓水肿的减轻。我们的结果表明,脊髓缺血/再灌注后AQP4蛋白的表达是区域特异性的,时间依赖性的,并且还表明,BK诱导的AQP4表达的减弱可能是脊髓缺血性水肿生理病理学的重要分子机制之一。 。

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