...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Biochemical and Biophysical Research Communications >MicroRNA-126-3p attenuates blood-brain barrier disruption, cerebral edema and neuronal injury following intracerebral hemorrhage by regulating PIK3R2 and Akt
【24h】

MicroRNA-126-3p attenuates blood-brain barrier disruption, cerebral edema and neuronal injury following intracerebral hemorrhage by regulating PIK3R2 and Akt

机译：通过调节PIK3R2和AKT，MicroRNA-126-3P衰减血脑屏障中断，脑水肿和神经元损伤后脑内出血

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Abstract MiR-126, a microRNA implicated in blood vessel integrity, angiogenesis and vascular inflammation, is markedly decreased in the sera of patients with intracerebral hemorrhage (ICH). The current study aims to evaluate the potential therapeutic effect of miR-126-3p on brain injuries in a rat model of collagenase-induced ICH. Intracerebroventricular administration of a miR-126-3p mimic significantly alleviated behavioral defects 24?h after ICH, as examined by paw placement and corner tests. ICH led to increased blood-brain barrier (BBB) permeability and cerebral edema, both of which were attenuated by miR-126-3p mimic. Treatment with miR-126-3p mimic reduced the numbers of myeloperoxidase (MPO)-positive, OX42-positive, Fluoro Jade B (FJB)-positive and NEUN/TUNEL double-positive cells around the hematoma, implying that miR-126-3p inhibited neutrophil infiltration, microglial activation and neuronal apoptosis following hemorrhage. In addition, miR-126-3p mimic suppressed the upregulation of phosphoinositide-3-kinase regulatory subunit 2 (PIK3R2) in the perihematomal area and maintained the activation of Akt. Furthermore, in?vitro assays confirmed upregulation of PIK3R2 upon knockdown of miR-126-3p in rat brain microvascular endothelial cells (BMECs), and silencing of miR-126-3p resulted in impaired BMEC barrier permeability and reversed vascular endothelial growth factor (VEGF)- and angiopoietin-1 (Ang-1)-induced activation of Akt and inhibition of BMEC apoptosis. In summary, our results suggest that exogenous miR-126-3p may alleviate BBB disruption, cerebral edema and neuronal injury following ICH by targeting PIK3R2 and the Akt signaling pathway in brain vascular endothelium. Highlights ? MiR-126-3p mimic improves behavioral performance and ameliorated neurological impairments after ICH. ? MiR-126-3p mimic inhibits neuron loss and attenuates inflammatory injury around the hematoma. ? MiR-126-3p mimic improves blood-brain barrier stability and regulates PIK3R2 and Akt.
机译：摘要MIR-126，血管完整性，血管生成和血管炎症的微小RORNA在脑出血（ICH）患者的血清中显着降低。目前的研究旨在评估miR-126-3p对胶原酶诱导的inch大鼠脑损伤脑损伤的潜在治疗效果。 MIR-126-3P的脑内施用MIR-126-3P在ICH之后显着减轻了24℃，如爪子放置和角落测试所检查。 ICH导致血脑屏障（BBB）渗透性和脑水肿增加，两者都被MIR-126-3P模仿衰减。用miR-126-3p治疗模仿肌晶酶（mpo） - 阳性，Ox42阳性，氟玉石（FJB） - 血肿周围的辐射和Neun / Tunel双阳性细胞周围的数量，这意味着mir-126-3p出血后抑制中性粒细胞浸润，小胶质激活和神经元细胞凋亡。此外，MiR-126-3P模仿抑制了磷酸阳性阳性-3-激酶调节亚基2（PIK3R2）的上调，并保持了AKT的活化。此外，在体外测定中，在大鼠脑微血管内皮细胞（BMEC）敲低MiR-126-3P时确认PIK3R2的上调，并且MiR-126-3P的沉默导致BMEC阻隔渗透率受损和逆转血管内皮生长因子（VEGF ） - 血管生成素-1（Ang-1） - 诱导AKT的激活和BMEC凋亡的抑制作用。总之，我们的结果表明，外源MiR-126-3P通过靶向PIK3R2和脑血管内皮中的AKT信号通路，可以缓解BBB破坏，脑水肿和神经元损伤。强调 ？ MiR-126-3P模仿在ICH后提高了行为性能和改善神经系统损伤。还MiR-126-3P模仿抑制神经元损失并衰减血肿周围的炎症损伤。还MiR-126-3P模仿改善了血脑屏障稳定性并调节Pik3R2和Akt。

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