中文摘要：

目的研究染料木黄酮（Gen）对β淀粉样肽25-35（Aβ25-35）介导的星形胶质细胞氧化损伤中Nrf2／ARE通路相关因子的调节作用。方法以星形胶质细胞（C6细胞系）作为研究对象，用Aβ25-35染毒制备氧化损伤模型。实验共分4组：对照组、Aβ组（Aβ模型组）、Gen干预组（Gen＋Aβ组）及Gen组（Gen单独处理组）；采用RT-PCR方法和WesternBlot方法检测星形胶质细胞核因子E2相关因子2（Nrf2）、血红素加氧酶（HO-1）、γ-谷氨酰半胱氨酸合成酶催化亚单位（GCLC）及锰超氧化物歧化酶（MnSOD）基因和蛋白的表达。结果与Aβ组比较，Gen干预组和Gen组星形胶质细胞Nrf2、HO-1、GCLC及MnSOD基因和蛋白表达水平显著上调（P〈0．05）。结论染料木黄酮可能通过调控Nrf2／ARE通路来拮抗Aβ25-35介导的星形胶质细胞氧化损伤作用。

英文摘要：

Objective The aim of this study was to investigate the effects of genistein （GEN） on the Nrf2/ARE pathway related factors during protection of oxidative damage induced by β-amyloid peptides （Aβ25-35） in astrocytes （ C6 cells）. Methods Astrocytes was cultured for 48hrs. Aβ25-35 （25p, mol/L） was used to establish oxidative damage model in astrocytes. Four groups are control group, Aβ group, Gen-treated group （ Gen ＋ Aβ group） and Gen group （ solo- Gen group）. Gen （50 μmol/L） was applied 2 hrs piror to the addition of Aβ25-35. After 24 hrs pretreatment, cells were harvested fur assays. The mRNA and protein expression of nuclear factor erythroid 2-related factor 2 （Nrf2） , heine oxygenase-1 （HO-1）, catalytic subunit of glutamate-cysteine ligase （GCLC） and manganese superoxide dismutase （MnSOD） in astrocytes were tested by RT-PCR and Western Bolt. Results Comparing with Aβ group, the mRNA and protein expression of Nrf2, HO-1, GCLC and MnSOD significantly increased in Gen-treated group and Gen group （ P 〈 0.05）. Conclusion Genistein could inhibit the oxidative damage induced by Aβ25-35 in astrocytes through regulating Nrf2/ARE pathway related factors.