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作 者:李娜[1] 曹翔[2] LI Na;CAO Xiang(Nanjing General Hospital of PLA,Nanjing University Medical School,Nanjing,Jiangsu 210002,China)
机构地区:[1]东部战区总医院(原南京军区南京总医院)输血科,江苏南京210002 [2]南京大学医学院附属鼓楼医院神经内科,江苏南京210008
出 处:《中风与神经疾病杂志》2020年第10期868-871,共4页Journal of Apoplexy and Nervous Diseases
基 金:全军重大课题(No.ANJ13J001);国家自然科学基金(81701170);江苏省自然科学基金(BK20170122);南京总医院科研基金(No.2015051)。
摘 要:目的探讨二氢杨梅素对氧糖剥夺/再灌注(OGD/R)导致的神经元氧化应激损伤的影响和可能的作用机制。方法体外培养大脑皮质原代神经元细胞,建立OGD/R损伤细胞模型。利用不同浓度的二氢杨梅素处理神经元细胞,2’,7’-二氯荧光黄双乙酸盐(DCFH-DA)法检测细胞内活性氧(ROS)水平。以超氧化物歧化酶(SOD)和丙二醛(MDA)为细胞氧化水平的指标。细胞核质分离方法检测核因子E2相关因子(Nrf2)核/质转位情况,免疫印迹法检测血红素氧合酶1(HO-1)的蛋白表达。结果与OGD/R组相比,二氢杨梅素处理组细胞生存率显著提高,ROS和MDA水平降低,SOD活性增高。同时二氢杨梅素处理增高了HO-1的蛋白表达并影响Nrf2的核质转位。结论二氢杨梅素通过激活Nrf2/HO-1抗氧化通路抑制OGD/R所致的原代神经元细胞氧化应激损伤。Objective To investigate the effect and potential mechanism of ampelopsin on oxygen-glucose deprivation/reoxygenation(OGD/R)-induced oxidative stress in neurons.Methods Primary cortical neurons were prepared from 15~17 days C57/BL6J mice embryos and OGD/R model was applied to primary cortical neurons cell.Different concentrations of ampelopsin were added to OGD/R-treated neurons.Intracellular ROS production was measured using the DCFH-DA method.Oxidative stress indicators were detected by malondialdehyde(MDA)and superoxide dismutase(SOD).The expression of nuclear factor erythroid 2-related factor 2(Nrf2)and heme oxygenase 1(HO-1)were detected by western blotting.Results Compared with the OGD/R group,ampelopsin promoted the survival of neurons exposed to OGD/R,decreased the levels of ROS and MDA while increased SOD activity.Meanwhile,ampelopsin treatment significantly inhibited nucleus to cytoplasm translocation of Nrf2 and increased the expression of HO-1 in neurons.Conclusion Treatment with ampelopsin before OGD/R alleviated oxidative stress damage through activating Nrf2/HO-1 signaling pathways.
关 键 词:神经元 氧化应激损伤 氧糖剥夺/再灌注 二氢杨梅素
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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