...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >The neuroprotective mechanism of ampicillin in a mouse model of transient forebrain ischemia
【24h】

The neuroprotective mechanism of ampicillin in a mouse model of transient forebrain ischemia

机译：氨苄西林在短暂性前脑缺血小鼠模型中的神经保护机制

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Ampicillin, a β-lactam antibiotic, dose-dependently protects neurons against ischemic brain injury. The present study was performed to investigate the neuroprotective mechanism of ampicillin in a mouse model of transient global forebrain ischemia. Male C57BL/6 mice were anesthetized with halothane and subjected to bilateral common carotid artery occlusion for 40 min. Before transient forebrain ischemia, ampicillin (200 mg/kg, intraperitoneally [i.p.]) or penicillin G (6,000 U/kg or 20,000 U/kg, i.p.) was administered daily for 5 days. The pretreatment with ampicillin but not with penicillin G signifi cantly attenuated neuronal damage in the hippocampal CA1 subfield. Mechanistically, the increased activity of matrix metalloproteinases (MMPs) following forebrain ischemia was also attenuated by ampicillin treatment. In addition, the ampicillin treatment reversed increased immunoreactivities to glial fibrillary acidic protein and isolectin B4, markers of astrocytes and microglia, respectively. Furthermore, the ampicillin treatment significantly increased the level of glutamate transporter-1, and dihydrokainic acid (DHK, 10 mg/kg, i.p.), an inhibitor of glutamate transporter-1 (GLT-1), reversed the neuroprotective effect of ampicillin. Taken together, these data indicate that ampicillin provides neuroprotection against ischemia-reperfusion brain injury, possibly through inducing the GLT-1 protein and inhibiting the activity of MMP in the mouse hippocampus.
机译：β-内酰胺抗生素氨苄青霉素可剂量依赖性地保护神经元免受缺血性脑损伤。进行本研究以研究氨苄青霉素在短暂性前脑缺血的小鼠模型中的神经保护机制。用氟烷麻醉雄性C57BL / 6小鼠，并使其双侧颈总动脉闭塞40分钟。在短暂性前脑缺血之前，每天给予氨苄青霉素（200 mg / kg，腹膜内[i.p.]）或青霉素G（6,000 U / kg或20,000 U / kg，i.p。），持续5天。用氨苄西林而不用青霉素G预处理可显着减轻海马CA1子区的神经元损伤。从机理上讲，氨苄青霉素治疗也可减轻前脑缺血后基质金属蛋白酶（MMPs）活性的增加。此外，氨苄西林治疗逆转了对星形胶质细胞和小胶质细胞标记物神经胶质纤维酸性蛋白和异凝集素B4免疫反应的增强。此外，氨苄青霉素治疗显着增加了谷氨酸转运蛋白-1的水平，二氢海藻酸（DHK，10 mg / kg，腹腔注射），一种谷氨酸转运蛋白-1的抑制剂（GLT-1），逆转了氨苄西林的神经保护作用。综上所述，这些数据表明氨苄青霉素可能通过诱导GLT-1蛋白和抑制小鼠海马中MMP的活性而提供了针对缺血再灌注脑损伤的神经保护作用。

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