首页> 外文期刊>Artificial Organs >Hydrogen Gas Ameliorates Hepatic Reperfusion Injury After Prolonged Cold Preservation in Isolated Perfused Rat Liver
【24h】

Hydrogen Gas Ameliorates Hepatic Reperfusion Injury After Prolonged Cold Preservation in Isolated Perfused Rat Liver

机译:氢气长期隔离保存的大鼠肝脏保冷后可减轻肝脏再灌注损伤

获取原文
获取原文并翻译 | 示例
           

摘要

Hydrogen gas reduces ischemia and reperfusion injury (IRI) in the liver and other organs. However, the precise mechanism remains elusive. We investigated whether hydrogen gas ameliorated hepatic I/R injury after cold preservation. Rat liver was subjected to 48-h cold storage in University of Wisconsin solution. The graft was reperfused with oxygenated buffer with or without hydrogen at 378 for 90 min on an isolated perfusion apparatus, comprising the H-2(+) and H-2 (-) groups, respectively. In the control group (CT), grafts were reperfused immediately without preservation. Graft function, injury, and circulatory status were assessed throughout the perfusion. Tissue samples at the end of perfusion were collected to determine histopathology, oxidative stress, and apoptosis. In the H-2(-) group, IRI was indicated by a higher aspartate aminotransferase (AST), alanine aminotransferase (ALT) leakage, portal resistance, 8-hydroxy-2-deoxyguanosine-positive cell rate, apoptotic index, and endothelial endothelin-1 expression, together with reduced bile production, oxygen consumption, and GSH/GSSG ratio (vs. CT). In the H-2(+) group, these harmful changes were significantly suppressed [vs. H-2(-)]. Hydrogen gas reduced hepatic reperfusion injury after prolonged cold preservation via the maintenance of portal flow, by protecting mitochondrial function during the early phase of reperfusion, and via the suppression of oxidative stress and inflammatory cascades thereafter.
机译:氢气可减少肝脏和其他器官的缺血和再灌注损伤(IRI)。但是,精确的机制仍然难以捉摸。我们研究了冷藏后氢气是否能改善肝脏I / R损伤。大鼠肝在威斯康星大学溶液中进行48小时冷藏。在隔离的灌注设备上,分别在包含H-2(+)和H-2(-)的单独灌注设备上,在378处用含氧缓冲液(含氢或不含氢)对移植物再灌注90分钟。在对照组(CT)中,立即将移植物再灌注而不保存。在整个灌注过程中评估移植物功能,损伤和循环状态。在灌注结束时收集组织样品以确定组织病理学,氧化应激和凋亡。在H-2(-)组中,较高的天冬氨酸转氨酶(AST),丙氨酸转氨酶(ALT)渗漏,门静脉阻力,8-羟基-2-脱氧鸟苷阳性细胞率,凋亡指数和内皮素表示IRI -1表达,以及降低的胆汁产量,耗氧量和GSH / GSSG比(相对于CT)。在H-2(+)组中,这些有害变化得到了显着抑制[vs. H-2(-)]。氢气通过维持门脉血流,在再灌注早期保护线粒体功能以及随后抑制氧化应激和炎症级联反应,从而在长期保冷后减少了肝脏的再灌注损伤。

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