...
首页> 外文期刊>CNS neuroscience & therapeutics. >Molecular Hydrogen Suppresses Reactive Astrogliosis Related to Oxidative Injury during Spinal Cord Injury in Rats
【24h】

Molecular Hydrogen Suppresses Reactive Astrogliosis Related to Oxidative Injury during Spinal Cord Injury in Rats

机译:分子氢抑制大鼠脊髓损伤过程中与氧化损伤相关的反应性星形胶质沉着。

获取原文
           

摘要

Summary Aims Spinal cord injury ( SCI ) can induce excessive astrocyte activation. Hydrogen has been deemed as a novel antioxidant. We investigated whether molecular hydrogen could act as an antiastrogliosis agent during SCI and oxidative injury in experimental rats and cultured astrocytes. Methods Hydrogen‐rich saline ( HS , 8 mL/kg, i.p.) was injected every 12 h after SCI in rats. The expression of STAT 3, p‐ STAT 3, and glial fibrillary acidic protein ( GFAP ); the release of IL ‐1 β , IL ‐6, and TNF ‐ α ; and astrogliosis, along with the BBB score, were evaluated. Culturing astrocytes with hydrogen‐rich medium, the intracellular reactive oxygen species ( ROS ), astrogliosis, and the release of proinflammatory cytokines were assessed after H2O2‐induced injury. Results In the HS group, the expression of STAT 3, p‐ STAT 3, and GFAP and the proinflammatory cytokines were decreased in local spinal cord on postoperation day ( POD ) 3; on POD s 7 and 14, reactive astrogliosis was suppressed, and the locomotor function was also improved. Furthermore, hydrogen‐rich medium attenuated the intracellular production of ROS (especially HO ?), astrogliosis, and the secretion of proinflammatory cytokines in astrocytes 12 h after H2O2‐induced injury. Conclusions Molecular hydrogen could suppress reactive astrogliosis after contusive SCI and reduce the release of proinflammatory cytokines produced by active astrocytes related to oxidative injury. Thus, molecular hydrogen is potential to be a neuroprotective agent.
机译:概述目的脊髓损伤(SCI)可以诱导星形胶质细胞过度活化。氢被认为是一种新型的抗氧化剂。我们调查了在实验大鼠和培养的星形胶质细胞中,SCI和氧化损伤期间分子氢是否可以充当抗星形胶质细胞增生剂。方法大鼠SCI后每12小时注射一次富氢盐水(HS,8 mL / kg,腹腔注射)。 STAT 3,p-STAT 3和神经胶质纤维酸性蛋白(GFAP)的表达; IL-1β,IL-6和TNF-α的释放;评估了星形胶质细胞增多症和星形胶质细胞沉着症。在H2O2诱导的损伤后,用富含氢的培养基培养星形胶质细胞,评估细胞内活性氧(ROS),星形胶质细胞增多和促炎细胞因子的释放。结果在HS组,术后第3天,局部脊髓中STAT 3,p-STAT 3和GFAP的表达以及促炎细胞因子减少;在POD s 7和14上,反应性星形胶质增生受到抑制,运动功能也得到改善。此外,富氢培养基可减弱H2O2诱导的损伤后12小时星形胶质细胞中ROS(尤其是HO?),星形胶质细胞增多和促炎细胞因子分泌的细胞内产生。结论分子氢可以抑制挫伤性脊髓损伤后反应性星形胶质细胞增生,并减少活性星形胶质细胞产生的与氧化损伤有关的促炎细胞因子的释放。因此,分子氢有可能成为神经保护剂。

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