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目的探讨核因子相关因子2(Nrf2)/抗氧化反应元件(ARE)通路对T2DM大鼠胰岛β细胞功能的影响及其与胰岛素受体底物-2(IRS-2)表达的关系。方法雄性Wistar大鼠随机分为正常对照组(NC)、糖尿病模型组(DM)及叔丁基对苯二酚干预组(DM+tBHQ)。连续干预8周,评测胰岛β细胞功能及相关检测。结果 DM+tBHQ组胰岛β细胞功能、总超氧化物歧化酶(T-SOD)浓度、Nrf2、IRS-2蛋白表达及IRS-2磷酸化程度较DM组升高;丙二醛(MDA)、TNF-α浓度较DM组降低(P=0.000)。结论激活Nrf2/ARE通路可通过上调Nrf2下游靶基因在胰岛β细胞中的表达,以减轻氧化应激和慢性炎症反应对IRS-2的进一步损伤,从而延缓胰岛β细胞功能衰退。
Objective To investigate the effect of nuclear factor 2 (Nrf2) / antioxidant (ARE) pathway on islet β cell function and its relationship with insulin receptor substrate-2 (IRS-2) expression in T2DM rats. Methods Male Wistar rats were randomly divided into normal control group (DM), diabetic model group (DM) and tert-butyl hydroquinone intervention group (DM + tBHQ). Continuous intervention for 8 weeks, assessment of pancreatic β-cell function and related testing. Results The levels of beta-cell function, total superoxide dismutase (T-SOD), Nrf2, IRS-2 protein and IRS-2 phosphorylation were increased in DM + tBHQ group compared with those in DM group. MDA, The concentration of TNF-α was lower than that of DM group (P = 0.000). Conclusion Activation of Nrf2 / ARE pathway can delay the decline of pancreatic β-cell function by up-regulating the expression of downstream targets of Nrf2 in pancreatic β-cells, so as to reduce the further damage of oxidative stress and chronic inflammatory response to IRS-2.