| 魏敏1,2 闫志强3 董明清1 刘曼玲1 罗颖1 杨江河3 李志超1.丹参酮ⅡA 预防慢性缺氧大鼠认知功能障碍的电生理机制[J].,2012,12(11):2057-2060 |
| 丹参酮ⅡA 预防慢性缺氧大鼠认知功能障碍的电生理机制 |
| The Electrophysiological Mechanism of Tanshinone ⅡA Preventing ChronicHypobaric Hypoxia -Induced Cognitive Deficits |
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| DOI： |
| 中文关键词: 慢性缺氧 丹参酮ⅡA 认知功能障碍 电生理 |
| 英文关键词: Hypobaric hypoxia TanshinoneⅡA Cognitive deficits Electrophysiology |
| 基金项目: |
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| 中文摘要: |
| 目的：探讨丹参酮ⅡA (TⅡA) 预防慢性缺氧大鼠认知功能障碍的电生理机制。方法：将18 只雄性SD 大鼠(200-250 g)随机
分为对照组、模型组(Model 组) 、TⅡA(10mg/kg·d)治疗组(TⅡA 组)。复制慢性缺氧大鼠认知功能障碍模型，并给予相应治疗，在
脑片水平运用膜片钳技术检测海马CA1 区的LTP 变化，并检测海马CA1 区锥体细胞的兴奋性变化。结果：(1) 给予高频强直刺激
（HFS）后各组兴奋性突出后电位（fEPSP）斜率均显著增加，即均可诱发LTP 并持续1h 以上，但模型组LTP 较对照组显著减弱
（P<0.05），TⅡA 治疗组LTP 较模型组明显增强（P<0.05）；(2) 慢性缺氧使海马CA1 锥体细胞放电所需的刺激电流幅度显著增加、
阈电位升高、兴奋性降低，同样刺激强度条件下动作电位数量减少，TⅡA 干预可明显减轻慢性缺氧对海马CA1 锥体细胞的上述
抑制。结论：TⅡA 可能是通过维持海马CA1 锥体细胞的兴奋性、维持海马的突出可塑性减轻慢性缺氧对认知功能的损害。 |
| 英文摘要: |
| Objective: To investigate the electrophysiological mechanism of Tanshinone ⅡA (TⅡA) preventing cognitive deficits
induced by chronic hypobaric hypoxia. Methods: Eighteen male Sprague-Dawley rats (200-250 g) were randomly divided into three
groups (n=6): Control group, Model group and TⅡA group. Hippocampal CA1 LTP was detected by patch-clamp recordings in rat brain
slices. Excitability of Hippocampal CA1 pyramidal neurons was measured by whole-cell patch-clamp recordings. Results: The LTP of
hippocampal CA1 was inhibitted by chronic hypobaric hypoxia, and TⅡA can maintain the LTP. The decrease of excitability of hippocampal
CA1 pyramidal neurons caused by chronic hypobaric hypoxia was markedly improved by TⅡA. Conclusions: TⅡA can prevent
cognitive deficits caused by chronic hypobaric hypoxia via maintaining the excitability of hippocampal CA1 pyramidal neurons. |
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