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  • Title: [Effect of EGCG on oxidative stress and Nrf2/HO-1 pathway in neurons exposed to oxygen-glucose deprivation/reperfusion].
    Author: He F, Zhang Y, Chen S, Ye B, Chen J, Li C.
    Journal: Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2018 Oct 28; 43(10):1041-1047. PubMed ID: 30523222.
    Abstract:
    To explore the effect of epigallocatechin gallate (EGCG) on oxidative stress and Nrf2/HO-1 pathway in neurons subjected to oxygen-glucose deprivation/reperfusion (OGD/R).
 Methods: Primary cultured cerebral cortical neurons were prepared from Sprague-Dawley rats, and the OGD/R cell model was established. After pretreatment with EGCG at different concentrations (12.5, 25.0, 50.0 or 100.0 μmol/L), the neurons were subjected to OGD/R. The cell viability, reactive oxygen species (ROS) level and malondialdehyde (MDA) content were assessed after reperfusion. The superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were measured. The expression of Nrf2 protein in nucleus, HO-1 mRNA and protein were detected.
 Results: OGD/R treatment reduced the cell viability, elevated ROS level and MDA content, decreased SOD and GSH-Px activities. The expression of Nrf2 protein in nucleus, HO-1 mRNA and protein were increased (P<0.01). Pretreatment with EGCG promoted the survival of neurons exposed to OGD/R, decreased ROS level and MDA content while increased SOD and GSH-Px activities. The levels of Nrf2 protein in nucleus, HO-1 mRNA and protein were upregulated (P<0.01).
 Conclusion: EGCG can reduce the oxidative stress of neurons subjected to OGD/R, which may be related to activation of Nrf2/HO-1 signal pathway and enhancement of the antioxidant ability of neurons. 目的：研究表没食子儿茶素没食子酸酯(epigallocatechin gallate，EGCG)对氧糖剥夺/再灌注(oxygen-glucose deprivation/reperfusion，OGD/R)导致的神经元氧化应激损伤及核因子E2-相关因子2(nuclear factor erythroid 2-related factor 2，Nrf2)/血红素加氧酶-1(heme oxygenase-1，HO-1)通路的影响。方法：取原代培养的大鼠大脑皮层神经元，建立OGD/R损伤细胞模型。于OGD/R前加入不同浓度(12.5，25.0，50.0，100.0 μmol/L)EGCG，再灌注后，测定细胞活力、活性氧(ROS)水平、丙二醛(MDA)含量、超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性，检测HO-1 mRNA，HO-1蛋白及细胞核Nrf2蛋白表达水平。结果：OGD/R导致神经元细胞活力降低，ROS水平和MDA含量升高，SOD和GSH-Px活性降低，HO-1 mRNA，HO-1蛋白及细胞核Nrf2蛋白表达增多(P<0.01)。EGCG能明显促进OGD/R神经元存活，降低ROS水平和MDA含量，提高SOD和GSH-Px活性，上调HO-1 mRNA，HO-1蛋白及细胞核Nrf2蛋白表达水平(P<0.01)。结论：EGCG能减轻OGD/R诱导的神经元氧化应激损伤，可能与激活Nrf2/HO-1信号通路，增强神经元的抗氧化能力有关。.
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