畜牧兽医学报 ›› 2021, Vol. 52 ›› Issue (8): 2302-2308.doi: 10.11843/j.issn.0366-6964.2021.08.023

• 基础兽医 • 上一篇    下一篇

右美托咪定对氯胺酮致发育期大鼠神经损伤的影响

张志恒, 白荟, 申美伦, 马相影, 李柔茜, 金箫笛, 高利*   

  1. 东北农业大学动物医学学院 黑龙江省实验动物与比较医学重点实验室, 哈尔滨 150030
  • 收稿日期:2020-12-18 出版日期:2021-08-23 发布日期:2021-08-21
  • 通讯作者: 高利,主要从事动物肢蹄病和麻醉药物研究,E-mail:gaoli43450@163.com
  • 作者简介:张志恒(1992-),男,内蒙古乌兰察布人,博士生,主要从事兽医麻醉与镇痛研究,E-mail:449756020@qq.com
  • 基金资助:
    国家自然科学基金(31372491;31572580);国家重点研发计划项目(2017YFD0501601-2)

Effects of Dexmedetomidine on Ketamine Induced Nerve Injury in Developing Rats

ZHANG Zhiheng, BAI Hui, SHEN Meilun, MA Xiangying, LI Rouqian, JIN Xiaodi, GAO Li*   

  1. Heilongjiang Key Laboratory Animals and Comparative Medicine, College of Animal Medicine, Northeast Agricultural University, Harbin 150030, China
  • Received:2020-12-18 Online:2021-08-23 Published:2021-08-21

摘要: 本研究旨在探讨右美托咪定干预氯胺酮致发育期大鼠神经损伤的影响及其可能的机制。7日龄SD大鼠随机分为对照组、氯胺酮组(氯胺酮20 mg·kg-1腹腔注射,每1.5 h注射1次,共5次)、右美托咪定组(右美托咪定腹腔注射15 μg·kg-1)和氯胺酮+右美托咪定组(氯胺酮注射前30 min,腹腔注射15 μg·kg-1右美托咪定)。最后1次给药90 min后,取大脑组织固定后进行尼氏染色;测定海马和皮质组织中CAT、GSH、MDA、IL-1β和IL-18的含量。尼氏染色结果显示,与对照组相比右美托咪定预先用药可以缓解氯胺酮导致的海马CA1区、CA3区和皮质区的神经元丢失。右美托咪定预处理还可以显著降低(P<0.05)海马和皮质MDA、IL-1β和IL-18水平,显著增加(P<0.05)CAT和GSH含量。综上表明,右美托咪定预处理能够有效降低海马和皮质MDA水平、增加CAT和GSH含量,并抑制炎症因子IL-1β和IL-18的分泌,在氯胺酮致发育期大鼠神经损伤时发挥神经保护作用。

关键词: 氯胺酮, 右美托咪定, 发育期大鼠, 认知功能障碍, 氧化应激

Abstract: The purpose of this study was to investigate the effect of dexmedetomidine on ketamine induced nerve injury in developing rats and its possible mechanism. Seven-day-old SD rats were randomly divided into control groups; ketamine group (20 mg·kg-1 ketamine, i.p. once every 1.5 hours, 5 times); dexmedetomidine group (15 μg·kg-1 dexmedetomidine, i.p); ketamine + dexmedetomidine group (30 min before ketamine injection, 15 μg·kg-1 dexmedetomidine, i.p.). Ninety minutes after the last administration, the brain tissue was taken and fixed for Nissl staining; the contents of CAT, GSH, MDA, IL-1β and IL-18 in the hippocampus and cortical tissue were measured. The results of Nissl staining showed that pre-administration of dexmedetomidine could alleviate the loss of neurons in hippocampal CA1, CA3, and cortex caused by ketamine compared with the control group. Dexmedetomidine pretreatment could also significantly reduce (P<0.05) the levels of MDA, IL-1β and IL-18 in the hippocampus and cortex, and significantly increase (P<0.05) the content of CAT and GSH. The results of the study show that dexmedetomidine pretreatment can effectively reduce hippocampal and cortical MDA levels, increase CAT and GSH content, and inhibit the secretion of IL-1β and IL-18, and exert neuroprotection when ketamine-induced neurological damage in developmental rats.

Key words: ketamine, dexmedetomidine, developmental rats, cognitive dysfunction, oxidative stress

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