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为了探讨一氧化氮 (NO)在缺血神经元坏死中的作用机制及三七总皂甙 (PNS)是否通过影响NO的变化而起脑保护作用。 方法 用栓线法建立大鼠局灶性脑缺血模型 ,测定脑缺血后不同时间脑组织NO含量和一氧化氮合成酶 (NOS)活性变化及PNS对其的影响。 结果 缺血后 3 0分钟脑组织NO含量和NOS活性均显著升高 (P <0 0 1 ) ,而PNS能防止脑缺血后两者的升高。NO含量与NOS活性呈显著正相关。 结论 NO在缺血神经元损伤中起重要作用 ,PNS是通过降低NO的含量而起保护脑组织作用
In order to investigate the mechanism of nitric oxide (NO) in ischemic neuronal necrosis and whether Panax Notoginseng Saponins (PNS) play a neuroprotective role by affecting the changes of NO. Methods The model of focal cerebral ischemia in rats was established by suture method. The content of NO and the activity of nitric oxide synthase (NOS) in brain tissue were measured at different time points after cerebral ischemia, and the effect of PNS on it. Results At 30 minutes after ischemia, the content of NO and the activity of NOS in brain tissue were significantly increased (P <0.01), while PNS could prevent both of them from rising after cerebral ischemia. There was a significant positive correlation between NO content and NOS activity. Conclusions NO plays an important role in ischemic neuronal injury. PNS plays a role in protecting brain tissue by decreasing the content of NO