首页> 美国卫生研究院文献>Oxidative Medicine and Cellular Longevity >Preexposure to Olive Oil Polyphenols Extract Increases Oxidative Load and Improves Liver Mass Restoration after Hepatectomy in Mice via Stress-Sensitive Genes
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Preexposure to Olive Oil Polyphenols Extract Increases Oxidative Load and Improves Liver Mass Restoration after Hepatectomy in Mice via Stress-Sensitive Genes

机译:暴露于橄榄油中的多酚提取物可通过应激敏感基因增强小鼠肝切除术后的氧化负荷并改善肝脏的质量恢复。

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摘要

Polyphenols can act as oxidants in some conditions, inducing redox-sensitive genes. We investigated the effect of preexposure to the olive oil polyphenols extract (PFE) on time-dependent changes in the hepatic oxidative state in a model of liver regeneration—a process in which oxidative stress associated with the metabolic overload accounts for the early events that contribute to the onset of liver self-repair. Liver regeneration was induced by one-third hepatectomy in mice. Prior to hepatectomy, mice were intraperitoneally given either PFE (50 mg/kg body weight) or saline for seven consecutive days, while respective controls received vehicle alone. Redox state-regulating enzymes and thiol proteins along with the mRNA levels of Nrf2 gene and its targets γ-glutamylcysteine synthetase and heme oxygenase-1 were determined at different time intervals after hepatectomy. The liver mass restoration was calculated to assess hepatic regeneration. The resulting data demonstrate the effectiveness of preexposure to PFE in stimulating liver regeneration in a model of a small tissue loss which may be ascribed to the transient increase in oxidant load during the first hours after hepatectomy and associated induction of stress response gene-profiles under the control of Nrf2.
机译:在某些情况下,多酚可作为氧化剂,诱导氧化还原敏感基因。在肝脏再生模型中,我们研究了橄榄油多酚提取物(PFE)的预暴露对肝脏氧化状态随时间变化的影响,该过程中与代谢超负荷相关的氧化应激是导致早期事件的原因。到肝脏自我修复开始。三分之一的小鼠接受肝切除术诱导肝脏再生。肝切除术前,连续7天给小鼠腹膜内给予PFE(50μmg/ kg体重)或生理盐水,而各对照组则单独接受赋形剂。在肝切除后的不同时间间隔,测定氧化还原状态调节酶和硫醇蛋白以及Nrf2基因的mRNA水平及其靶标γ-谷氨酰半胱氨酸合成酶和血红素加氧酶-1。计算肝脏质量恢复以评估肝再生。结果数据表明,在小组织损失模型中,预暴露于PFE可以有效地刺激肝脏再生,这可能归因于肝切除术后最初几个小时内氧化剂负荷的瞬时增加以及在此条件下相关的应激反应基因谱的诱导。 Nrf2的控制。

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