中文摘要：

目的：评价鼠尾草酸对H2O2损伤神经元的保护作用,并检测鼠尾草酸在不同保存条件下稳定性。方法：鼠尾草酸预处理体外培养C57小鼠胎鼠神经元,加入H2O2继续培养,神经元标志性抗体Tuj1染色,显微镜观察细胞状态并采用细胞活性（CCK-8）检测神经元的活性,生化法测定乳酸脱氢酶（LDH）释放量和丙二醛（MDA）、超氧化物歧化酶（SOD）的活性,实时荧光定量聚合酶链式反应（RT-PCR）检测神经元凋亡相关基因Caspase-3 mRNA的表达。同时,HPLC测定0~120 h不同保存条件下鼠尾草酸含量。结果：与模型组比较,20、80μmol/L浓度鼠尾草酸预处理组细胞状态好于模型组,细胞活性增强,培养液中LDH的漏出量降低,细胞内MDA的生成减少,SOD活性增强,caspase-3 mRNA表达显著下调;不同保存条件下鼠尾草酸含量随时间延长呈递差性降低。结论：鼠尾草酸对H2O2所致神经元的损伤具有保护作用,但稳定性差。

英文摘要：

Objective： To investigate the protective effect of carnosic acid on neurons damaged by H2O2 and detect its stability under different storage conditions. Methods： Neuron was treated with carnosic acid for 30 min prior to H2O2（ 50. 0 μmol/L） treatment. After 6 h,neuron morphology was observed by ICC using microscope,cell viability was tested with CCK-8,LDH,MDA level and SOD viability were measured by biochemical methods,caspase-3 mRNA expression was measured by RT-PCR. Meanwhile,we measured the content of Carnosic acid by HPLC in 0 ~ 120 h under different storage conditions. Results： Compare to the control group,neuron and SOD viability decreased（ P 〈 0.05） while LDH,MDA and caspase-3 mRNA level increased（ P 〈 0. 05） in the model group,groups pretreated with Carnosic acid,neuron and SOD viability increased（ P 〈 0. 05）,while LDH,MDA and caspase-3 mRNA level decreased（ P 〈 0. 05）; the content of carnosic acid continues decrease under different storage conditions. Conclusion： carnosic acid can protect H2O2 induced neuronal injury,but poor stability.