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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。
Objective: To investigate the electrophysiological mechanism of Tanshinone ⅡA (TⅡA) in preventing cognitive impairment in chronic hypoxic rats. Methods: Eighteen male SD rats (200-250 g) were randomly divided into control group, Model group and TⅡA group (TⅡA group). The model of cognitive impairment in chronic hypoxia rats was duplicated and treated accordingly. The changes of LTP in hippocampal CA1 region were detected by patch-clamp technique at the level of brain slices. The excitability of pyramidal cells in hippocampal CA1 region was detected. Results: (1) After high-frequency tonic stimulation (HFS), the slope of esophageal epithelial potential (fEPSP) increased significantly, that is, LTP could be induced for more than 1 hour, but LTP in model group was significantly lower than that in control group (P <0.05); (2) LTP of TⅡA treatment group was significantly higher than that of model group (P <0.05); (2) The amplitude of stimulation current required for chronic hypoxia to discharge hippocampal CA1 pyramidal cells was significantly increased, the threshold potential was increased, Under the same stimulus intensity, the number of action potentials decreased, TIIA intervention could obviously reduce the above inhibition of hippocampal CA1 pyramidal cells by chronic hypoxia. CONCLUSION: TⅡA may protect the cognitive function of hippocampal CA1 pyramidal neurons by maintaining the excitability of hippocampal CA1 pyramidal cells and maintaining hippocampal prominent plasticity.