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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Western Blot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。
AIM To investigate the regulatory effect of genistein on the Nrf2 / ARE pathway-related factors in the oxidative damage of astrocytes induced by amyloid beta peptide 25-35 (Aβ25-35). Methods Astrocyte (C6 cell line) was used as the research object. Aβ25-35 was used to prepare the model of oxidative damage. The experimental group was divided into four groups: control group, Aβ group (Aβ model group), Gen intervention group (Gen + Aβ group) and Gen group (Gen alone treatment group); RT-PCR and Western Blot (Nrf2), heme oxygenase (HO-1), γ-glutamylcysteine synthase catalytic subunit (GCLC) and manganese superoxide dismutase (MnSOD) gene and Protein expression. Results Compared with Aβ group, the gene and protein expressions of Nrf2, HO-1, GCLC and MnSOD in Gen and Gen groups were significantly increased (P <0.05). Conclusion Genistein may antagonize Aβ25-35-mediated oxidative damage of astrocytes by regulating the Nrf2 / ARE pathway.