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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
Objective To observe the protective effect of Chinese herbal medicine Anti-dead I on cerebral cortex neurons in simulated cerebral ischemic reperfusion injury in rats. Methods Rat cerebral cortical neurons cultured in vitro were simulated for 4 h ischemia and reperfusion injury during ischemia and 3, 18, 24, 48 and 72 h after reperfusion. The activity, survival rate, mortality and lactate were observed. The leakage rate of hydrogenase (LDH) and the activity of nitric oxide synthase (NOS) and the effect of traditional Chinese medicine anti-dead I. Results With the prolongation of ischemia and reperfusion, the rat neurons cultured in vitro had a gradual decrease in cell viability, a gradual increase in mortality, a gradual increase in the leakage rate of LDH in the culture fluid, and an activity of NOS in the ischemic cells. Significantly higher at 4h and 3h after reperfusion. Anti-dead I can affect the changes in the above indicators. Conclusion Antideadol I may protect mitochondria by preventing dephosphorylation of oxidative phosphorylation, prevent lipid peroxidation and increase in permeability, protect cell membrane, and increase the reactivity of inhibiting NOS activity to prevent NO and its derived toxic free radicals. Damage, etc., and play a protective role against neurons