【摘要】 目的　观察中药抗呆Ⅰ号对体外模拟脑缺血再灌注损伤大鼠大脑皮层神经元的保护作用。方法　体外培养的大鼠大脑皮层神经元 ,模拟脑缺血再灌注损伤中缺血 4h及再灌 3、1 8、2 4、4 8、72h ,观察其活性、存活率、死亡率、乳酸脱氢酶 (LDH)的漏出率和一氧化氮合成酶 (NOS)的活性变化以及中药抗呆Ⅰ号的影响。结果　体外培养的大鼠大脑皮层神经元随缺血和再灌注时间的延长 ,细胞存活率逐渐下降、死亡率逐渐升高、培养液中LDH的漏出率逐渐升高 ,细胞NOS的活性在缺血 4h和再灌 3h时显著增高。抗呆Ⅰ号可影响其上述指标的变化。结论　抗呆Ⅰ号可能通过防止氧化磷酸化脱偶联而保护线粒体 ,防止脂质过氧化及通透性增加而保护细胞膜 ,抑制NOS活性的反应性增强而防止NO及其衍生的毒性自由基的损伤等 ,而发挥对神经元的保护作用更多还原

【Abstract】 Objective To observe the protective effects of Kangdai I on the cultivated rat cortical neurons damaged by mimic cerebral ischemia and reperfusion. Method the neuronal activity, survival rate, death rate, LDH leakage rate, the change in NOS activity, and the effects of Kangdai I were observed in the cultivated rat cortical neurons damaged by mimic cerebral ischemia of 4 hours and reperfusion for 3, 18, 24, 48 and 72 hours, respectively. Results Along with the ischemia and the prolonging of the time for reperfusion, a gradual decrease in the survival rate, a gradual increase in the death rate and in LDH leakage rate were found in the rat cultivated neurons; and an obvious increase in the NOS activity was found at 4 hours of ischemia and 3 hours of reperfusion. Kangdai I could affect the changes in these criteria. Conclusion Kangdai I maybe exert its protective effects on neurons by protecting the mitochondria from oxidative phosphorylation decoupling, protecting the cell membrane through halting lipid peroxidation and the increase in the permeability, and preventing the damage of NO and NO-derived toxic free radicals through inhibiting the enhance in the NOS reaction.更多还原