EGCG对过氧化氢所致神经元过氧化损伤的保护作用

目的研究表没食子儿茶素没食子酸酚(EGCG)对过氧化氢(H2O2)所致神经元过氧化损伤的保护作用。方法分离胚胎18d大鼠大脑皮质神经元,原代培养2d后分为4组:①正常细胞对照组;②药物对照组(正常细胞内加EGCG);③氧化损伤组(正常细胞内加H2O2);④损伤后药物治疗组(氧化损伤30min后加入EGCG)。各组细胞再培养36h后,进行神经元形态观察、细胞活性MTT分析及细胞中丙二醛(MDA)含量的检测。结果氧化损伤组神经元多崩解成碎片,突起不完整,细胞活性显著降低,MDA含量显著升高。而在损伤后药物治疗组,神经元胞体立体感较强,多数突起完整。细胞活性显著增高,而MDA含量则显著下降。结论EGCG可抑制羟基自由基的产生,从而保护H2O2氧化损害的神经

Protective effect of tea polyphenol (-)-epigallocatechin gallate on peroxidation-injured neurons acutely exposed to hydrogen peroxide

Objective To investigate the effect of tea polyphenol (-) -epigallocatechin gallate (EGCG)on peroxidation-injured neurons acutely exposed to hydrogen peroxide (H2O2). Methods Cortical neurons from embryonic 18 day rats were primarily cultured for 2 days, and divided into 4 groups: ①Normal neuron control group, ②Normal neuron with EGCG group, ③H2O2 -injured neuron group (normal neurons with the treatment of H2O2), and ④EGCG-treatment group (Injured neurons treated with EGCG 30 minutes after H2O2 administration). All the neurons in different groups were cultured for another 36 hours before the morphological changes, viability and malondialdehyde (MDA) production of these neurons were analyzed. Results Most of the neurons in H2O2-injured neuron group exposed to H2O2 were destroyed into debris without complete processes. The neuronal viability decreased significantly with an increased production of MDA. However , cultured neurons in EGCG-treatment group remained an almost normal morphology with a significant increase in the neuronal viability and declined MDA production. Conclusion The outcomes of the present study suggested that EGCG is capable of inhibiting the production of hydroxide radical, thus protecting neurons against peroxidative damage caused by H2O2.