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首页> 外文期刊>Alcohol >Influence of low-dose alcohol consumption on post-ischemic inflammation: Role of cystathionine gamma-lyase
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Influence of low-dose alcohol consumption on post-ischemic inflammation: Role of cystathionine gamma-lyase

机译：低剂量醇消耗对缺血后炎症的影响：胱硫脲γ-裂解酶的作用

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摘要

Low-dose alcohol consumption (LAC) has been shown to suppress post-ischemic inflammation and alleviate cerebral ischemia/reperfusion (UR) injury. Cystathionine gamma-Lyase (CSE) is one of the enzymes that endogenously produce hydrogen sulfide (H2S), which has an anti-inflammatory property at low concentration. We determined the potential role of CSE in the protective effect of LAC. Male C57BL/6J mice were divided into two groups, an ethanol group and a control group, and gavage fed with 0.7 g/kg/day ethanol or volume-matched water once a day for 8 weeks. Transient focal cerebral ischemia was induced by unilateral middle cerebral artery occlusion (MCAO) for 90 min. CSE inhibitors were intra-peritoneally given 30 min prior to the ischemia. Cerebral 102 injury, H2S production, adhesion molecules, IL-1 receptor accessory protein (IL-1 RAcP), IL-1 beta, microglial activation, and neutrophil infiltration were evaluated at 24 h of reperfusion. Eight-week ethanol feeding upregulated CSE in the cerebral cortex and reduced cerebral I/R injury. Moreover, ethanol increased post-ischemic H2S production and alleviated the post-ischemic inflammatory response (expression of adhesion molecules, 1L-1RAcP, IL-1 beta, microglial activation, and neutrophil infiltration) in the peri-infarct cerebral cortex. Both inhibitors of CSE, DL-Propargylglycine (PAG) and beta-cyano-L-alanine (BCA), abolished the protective effect of ethanol on cerebral I/R injury. In addition, PAG attenuated the inhibitory effect of ethanol on the post-ischemic inflammation. Thus, LAC may protect against cerebral 1/R injury by suppressing post-ischemic inflammation via an upregulated CSE. (C) 2018 The Authors. Published by Elsevier Inc.
机译：已显示低剂量醇消耗（LAC）抑制缺血后炎症和缓解脑缺血/再灌注（UR）损伤。胱硫胺γ-裂解酶（CSE）是内源性产生硫化氢（H2S）的酶之一，其在低浓度下具有抗炎性能。我们确定了CSE在Lac的保护作用中的潜在作用。将雄性C57BL / 6J小鼠分为两组，乙醇基团和对照组，饲喂0.7g / kg /天的乙醇或乙醇或体积匹配的水，每天持续8周。由单侧中间脑动脉闭塞（MCAO）诱导瞬态焦脑缺血90分钟。在缺血之前，CSE抑制剂在30分钟内腹膜内给出。在再灌注的24小时评估脑102损伤，H2S生产，粘附分子，IL-1受体辅助蛋白（IL-1谱系，微胶质激活和中性粒细胞渗透。八周的乙醇喂养脑皮层中的上调CSE，降低脑I / R损伤。此外，乙醇增加了缺血性H2S后产生的产量，并减轻了Peri-Infarct脑皮质中的缺血性炎症反应（表达粘附分子，1L-1RACP，IL-1β，小胶质激活和中性粒细胞渗透）。 CSE，DL-丙基甘氨酸（PAG）和β-氰基-L-丙氨酸（BCA）的抑制剂都废除了乙醇对脑I / R损伤的保护作用。此外，PAG减弱了乙醇对缺血性炎症的抑制作用。因此，LAC可以通过通过上调CSE抑制缺血性炎症来保护脑1 / R损伤。 （c）2018作者。 elsevier公司发布

著录项

  • 来源
    《Alcohol》 |2019年第2019期|共9页
  • 作者

    McCarter Kimberly D.; Li Chun; Li Jiyu; Xu Guodong; Sun Hong;

  • 作者单位

    Louisiana State Univ Hlth Sci Ctr Shreveport Dept Cellular Biol &

    Anat Shreveport LA 71105 USA;

    Louisiana State Univ Hlth Sci Ctr Shreveport Dept Cellular Biol &

    Anat Shreveport LA 71105 USA;

    Louisiana State Univ Hlth Sci Ctr Shreveport Dept Cellular Biol &

    Anat Shreveport LA 71105 USA;

    Louisiana State Univ Hlth Sci Ctr Shreveport Dept Cellular Biol &

    Anat Shreveport LA 71105 USA;

    Louisiana State Univ Hlth Sci Ctr Shreveport Dept Cellular Biol &

    Anat Shreveport LA 71105 USA;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 中毒及化学性损害;
  • 关键词

    Ethanol; Brain; Ischemia/reperfusion; Inflammation; Cystathionine gamma-lyase;

    机译：乙醇;脑;缺血/再灌注;炎症;胱硫胺γ-裂解酶;

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