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目的探讨染料木黄酮(GEN)对全脑缺血(GCI)大鼠海马CA1区神经元的神经保护作用及其可能的机制。方法建立大鼠4动脉结扎全脑缺血模型,实验动物随机分为假手术组(sham)、缺血再灌注组(I/R)、GEN处理组、ICI 182,780组和溶剂对照组。采用Fluoro-Jade B和神经元特异性核蛋白(NeuN)染色观察海马CA1区神经元存活情况,TUNEL技术观察海马CA1区神经元的凋亡。Morris水迷宫观察大鼠的空间学习和记忆功能。结果 GEN发挥神经保护作用的最佳剂量为1.0 mg/kg;与sham组相比,I/R组和溶剂对照组海马CA1区TUNEL阳性神经元数量显著增多(P<0.01),而1.0 mg/kg GEN可显著降低缺血后TUNEL阳性神经元数量(P<0.01);与I/R组相比,GEN能明显改善缺血后大鼠的空间学习和记忆能力。缺血前侧脑室给予ICI 182,780可显著降低GEN的神经保护作用(P<0.01)。结论低剂量(1.0mg/kg)GEN可显著降低缺血后大鼠海马CA1区神经元损伤,改善认知功能,其分子机制可能与雌激素受体活性密切相关。
Objective To investigate the neuroprotective effects of genistein (GEN) on neurons in hippocampal CA1 region of rats with global cerebral ischemia (GCI) and its possible mechanism. Methods The rat model of 4-AS ligation was established. The experimental animals were randomly divided into sham group, I / R group, GEN group, ICI 182,780 group and solvent control group. The survival of hippocampal CA1 neurons was observed by Fluoro-Jade B and NeuN staining. The apoptosis of hippocampal CA1 neurons was observed by TUNEL technique. Morris water maze to observe the spatial learning and memory function of rats. Results The best dosage of GEN for neuroprotection was 1.0 mg / kg. Compared with sham group, the number of TUNEL positive neurons in hippocampal CA1 region of I / R group and solvent control group increased significantly (P <0.01) kg GEN significantly reduced the number of TUNEL-positive neurons after ischemia (P <0.01). Compared with I / R group, GEN significantly improved the spatial learning and memory ability of rats after ischemia. ICI 182,780 administered to the anterior ischemic ventricle significantly reduced the neuroprotective effect of GEN (P <0.01). Conclusions Genistein (1.0 mg / kg) can significantly reduce neuronal damage and improve cognitive function in hippocampal CA1 region of rats after ischemia, and its molecular mechanism may be closely related to estrogen receptor activity.