| 赵京禹 费翔 郭徽 岳琦 邓城旗 郝建华.右美托咪定预处理对小鼠肠缺血再灌注损伤的作用研究[J].,2014,14(35):6823-6826 |
| 右美托咪定预处理对小鼠肠缺血再灌注损伤的作用研究 |
| Effect of Dexmedetomidine Pretreatment on IntestinalIschemia-reperfusion Injury in Mice |
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| DOI： |
| 中文关键词: 右美托咪定 缺血再灌注损伤 氧化应激 |
| 英文关键词: Dexmedetomidine Ischemia-reperfusion injury Oxidative stress |
| 基金项目: |
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| 中文摘要: |
| 目 的： 右美托咪定（ Dexmedetomidine, Dex）属于琢-2 肾上腺素能受体激动剂具有抗焦虑、催眠、镇痛 和交感神经阻滞作用 。 最
新研究发现右美托咪定对心脏和肺的缺血再灌注损伤具有显著的保护效应， 但是右美托咪定是否对肠缺血再灌注损伤具有保护
作用，迄今为止还没有相关研究。因 此， 本研究以小鼠为模型， 观察右美托咪定预处理对小鼠肠缺血再灌注损伤的影响。 方法： 建
立肠缺血再灌注损伤小鼠模型，并分为假手术组、缺血再灌注组和右美托咪定与 处理组。 不同 剂 量（ 10， 25, 50 和 100 滋g/kg）右美
托咪定预处理小鼠。 提取小鼠肠 组织 ，用 不 同 的 试剂 盒分别 测定超氧化物歧化酶 （ Superoxide Dismutase, SOD）， 丙二醛
（ Malondialdehyde， MDA）， 谷胱甘肽（ Glutathione, GSH），一氧化氮（ Nitric Oxide， NO）和髓过氧化物酶（ Myeloperoxidase， MPO）的
水平变化。 结果： 右美托咪定预处理可以显著提高肠缺血再灌注损伤小鼠的存活率并呈剂 量依赖性。 右美托咪定预处理（ 100
滋g/kg）抑制由肠缺血再灌注损伤引 起的不良效应， 包括 SOD 水平降低， MDA 水平升高， GSH 水平降低， NO 水平升高和 MPO 水
平升高。 结论： 我们的研究表明 右美托咪定可以提高小鼠肠缺血再灌注损伤的生存率， 并且抑制 氧化应激反应， 炎症细胞的活化
和侵润以及 NO 的水平， 对肠缺血再灌注损伤具有显著的保护效应。 本研究不仅进一步证实了 右美托咪定的广泛的药理活性， 而
且为肠缺血再灌注损伤的治疗提供了 潜在的治疗 药物，其进一步的药理效应和作用 机制值得进一步的研究。 |
| 英文摘要: |
| Objectivre:Dexmedetomidine belongs to alpha-2 adrenergic receptor agonist and processes a variety of pharmaceutical
functions including anti-depression, hypnosis, analgesia and sympathetic block. Recently, dexmedetomidine has been demonstrated to
have significant protective effect on myocardial and lung ischemia-reperfusion (I/R) injury. However, the role of Dexmedetomidine in
intestinal I/R injury hasn’ t been explored to date. Thus, this study was to investigate the effect and mechanisms of dexmedetomidine
pretreatment on intestinal I/R injury in mice.Methods:Intestinal model of ischemia/reperfusion injury was established, and the animals
were divided into three groups: sham group, ischemia/reperfusion group and dexmedetomidine pretreatment group. Different doses of
dexmedetomidine (1 0, 25, 50 and 1 00 滋g/kg) were pre-administrated. Effects of dexmedetomidine on intestinal I/R injury was evaluated
by myeloperoxidase (MPO), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH) and nitric oxide (NO) according
to different kit protocol.Results:Dexmedetomidine improved survival rate of mice subjected to intestinal I/R injury in a dose-dependent
manner. Dexmedetomidine pretreatment also attenuated the effects caused by I/R injury, which included decreased SOD and GSH and
increased MDA and MPO.Conclusion:Our study demonstrated that dexmedetomidine shows protective effects on intestinal I/R injury in
mice through modulation of oxidative stress, neutrophils infiltration and NO level. This study not only demonstrated the extensive
pharmacological activities of dexmedetomidine， but also provided a potential therapeutic drug for intestinal I/R injury implying that the
further protective effect and underlying mechanisms deserved further investigation. |
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