摘要
目的研究表没食子儿茶酚没食子酸酯(EGCG)对FeSO4和H2O2诱导神经细胞损伤的保护作用。方法采用FeSO4和H2O2作用产生自由基的方法诱导离体培养的小鼠胚鼠大脑皮层神经细胞损伤建立模型。倒置相差显微镜进行神经元形态学观察,中性红比色法和MTT法测定神经细胞的存活数量和活性,TBARS法和BCA法分别测定神经细胞中丙二醛(MDA)的水平和总蛋白合成的能力。结果与FeSO4和H2O2损伤组进行比较,EGCG增加了神经细胞的存活数量和活性,降低MDA的含量和提高了总蛋白的合成能力。EGCG显示出较强的抗氧化能力。结论EGCG对FeSO4和H2O2诱导神经细胞损伤有明显的保护作用,其作用机制可能源于EGCG清除自由基和抑制脂质过氧化过程。
Aim To observe the protective effects of epigallocatechin gallate (EGCG) on cortical neurons of embryonic mice the injury by FeSO4/H2O2 in vitro. Methods The cell injury model was established with FeSO4/H2O2 for 24 h. The process of the growth and morphology of the neurons were observed under phase contrast microscope in vitro. The cell survival was analyzed using colormetric neutral red assay. The cortical neuronal viability was analyzed using MTT assay. TBARS method was performed to detect the levels of Malondialdehyde(MDA) . The composing capacity of total protein was measured by BCA method. Results As compared with FeSO4/H2O2, EGCG enhanced the mouse cortical neuronal survivality and viability, decreased the levels of MDA and increased the composing capacity of total protein. Conclusion EGCG exerted protective effects on cortical neurons the injury induced by FeSO4/H2O2, which may be related to free radial scavenging activity and lipid peroxidation process being inhabited.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2008年第1期105-108,共4页
Chinese Pharmacological Bulletin
基金
国家教育部优秀青年教师资助项目(No2002-350)
国家中医药管理局资助项目(No04-05zp62)