| 殷俊茹,高龙飞,王彬荣,杨永慧,高昌俊,孙绪德.右美托咪定改善东莨菪碱导致的老年大鼠认知功能障碍[J].现代生物医学进展英文版,2017,17(31):6014-6017. |
| 右美托咪定改善东莨菪碱导致的老年大鼠认知功能障碍 |
| Dexmedetomidine Improves Cognitive Disfunction in Elderly Rats induced by Scopolamine |
| Received:March 22, 2017 Revised:April 18, 2017 |
| DOI：10.13241/j.cnki.pmb.2017.31.004 |
| 中文关键词: 右美托咪定 东莨菪碱 认知功能 氧化应激 炎症 |
| 英文关键词: Dexmedetomidine Scopolamine Cognitive function Oxidative stress Inflammation |
| 基金项目:国家自然科学基金项目（31570845） |
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| 中文摘要: |
| 摘要 目的：探讨右美托咪定对东莨菪碱导致的老年大鼠认知功能障碍的影响及可能的作用机制。方法：20月龄老年雄性SD大鼠随机分为3组 （n=15）：东莨菪碱组（Sco组），东莨菪碱+右美托咪定组（Dex组），对照组（Con 组）。Sco组给予东莨菪碱剂量为0.8 mg/kg，Dex组给予东莨菪碱0.8 mg/kg+右美托咪定20 μg/kg，Con组给予等体积生理盐水。给药后2 h进行Morris 水迷宫测试。所有测试结束后测定海马组织内氧化应激反应，选取指标为SOD，MDA；利用ELISA方法测定海马TNF-α，IL-1β含量。结果：Morris 水迷宫结果显示，与Sco组相比，Dex组在第3、4天时，大鼠的逃避潜伏时间明显缩短（P<0.05），平台区域的探索时间延长（P<0.05）。与Sco组相比，右美托咪定干预后，Dex组海马区域SOD含量明显升高，MDA含量明显降低(P<0.05），并且减轻了炎症因子TNF-α，IL-1β含量。结论：右美托咪定可有效减轻东莨菪碱导致的老年大鼠认知功能障碍，其机制可能涉及右美托咪定在大鼠海马区域的抗氧化应激和抗炎症反应。 |
| 英文摘要: |
| ABSTRACT Objective: To observe the effect of Dexmedetomidine on cognitive disfunction in elderly rats induced by scopolamine and explore its functionary mechanism. Methods: The male SD rats, 20-month-old, were randomly divided into 3 groups (Sco group), Scopolamine + Dexamethidine group (Dex group) and Control group (Con group), rats were given scopolamine 0.8 mg/kg in Sco group, rats were given scopolamine 0.8 mg/kg + dexmedetomidine 20 μg/kg in Dex group, rats were given the same volume of saline in Con group. Morris water maze was performed on rats 2 h after administration. The oxidative reaction in the hippocampus was measured after the test. The indexes were selected as SOD and MDA, and the content of TNF-α and IL-1β in hippocampus was determined by en- zyme-linked immunosorbent assay (ELISA). Results: Compared with Sco group, the escape latency of the rats in the Dex group was sig- nificantly decreased and the exploration time of the plateau region was significantly increased. Compared with the Sco group the content of SOD in the hippocampus of rats was significantly increased after dexmedetomidine treatment, and the levels of TNF-α and IL-1β were reduced. Conclusion: Dexmedetomidine can effectively reduce the cognitive impairment in elderly rats induced by scopolamine and its mechanism may involve the anti-oxidative stress and anti-inflammatory response of dexmedetomidine in the hippocampus of rats. |
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