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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。
OBJECTIVE: To evaluate the protective effect of carnosic acid on neurons injured by H2O2, and to determine the stability of carnosic acid under different storage conditions. Methods: The neurons of fetal rat C57 mice were pretreated with carnosic acid. Cultured with H2O2, the neurons were stained with Tuj1, the cell morphology was observed by microscope and the activity of neurons was detected by cell viability (CCK-8) (LDH) release and the activities of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured by real-time quantitative polymerase chain reaction (RT-PCR) Caspase-3 mRNA expression. Meanwhile, the content of carnosic acid in different storage conditions was determined by HPLC at 0 ~ 120 h. RESULTS: Compared with the model group, the cells in the 20 and 80μmol / L groups were better than the model group, the cell viability increased, the amount of LDH leakage in the culture medium decreased, the production of MDA in the cells decreased, the activity of SOD increased, The expression of caspase-3 mRNA was down-regulated significantly. The content of carnosic acid decreased with the prolongation of time under different storage conditions. CONCLUSION: Carnosic acid has a protective effect on H2O2-induced neuronal injury but its stability is poor.