摘要：采用胎龄18天大鼠海马神经元进行培养，第5天以黄嘌呤-黄嘌呤氧化酶(X-XO)体系建立氧自由基损伤模型，并分别给与人参皂甙(Gin)、超氧化物歧化酶(SOD)、Gin+SOD，观察氧自由基对神经元的损伤及Gin、SOD的保护作用，结果表明：氧自由基组细胞死亡率明显高于正常组(P<0.01)，各抗自由基组细胞死亡率接近正常组(P>0.05)，自由基组神经元细胞器严重受损，脂褐素增多，核变形偏位，胞浆与胞核比例减少，而各抗自由基组上述损伤减轻，提示Gin和SOD可增强神经元抗氧化能力，减轻氧自由基对神经元的损害。

Study on Hippocampal Neurons Damaged by Oxygen Free Radical and Protected by Ginsenonsides

zhang Peijun ,Lü Yongli,Lai Hong(Neuroanatomy Research Laboratory, Brain Research Institute, China Medical University, shenyang, 110001)

Abstract：Hippocampal neurons from 18d embryonic Wistar rat were cultured in vitro with xanthine-xanthinoxidase (x-xo) damaging model. Geinsenosidcs (Gin), super oxide dinutase (SOD) and Gin+SOD were applied separately on the same time. The motality rate of neurons under free radical was 16.8±2.97% for 24h and 38±5.40% for 48h, both higher than those in the normal group (P<0.01), while the anti-free radical groups were close to the normal one (P>0.05). The organelles of neurons in the free radical group were damaged, lipofuscin increased, nuclei displaced and malformed, nuclear cytoplasmic ratio elevated and inclusion found in nuclei, while thc damage in the normal and all anti-free-radical groups were slighter. This showed that free radical might damage neuronal membrane system, leading to deformity, and make the neurons dead in end, Gin and SOD might enhance the anti-oxidation of hippocampal neurons, delay neuronal senility and death.

Keywords：hippocampal neuron; oxygen free radical; ginsenosides参考文献：

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