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富硒酵母对铝诱导的小鼠肝脏脂质过氧化和炎症的保护作用。

Selenium-Rich Yeast protects against aluminum-induced peroxidation of lipide and inflammation in mice liver.

机构信息

College of Science and Engineering, Foshan University, Foshan, 528231, Guangdong, People's Republic of China.

出版信息

Biometals. 2018 Dec;31(6):1051-1059. doi: 10.1007/s10534-018-0150-2. Epub 2018 Oct 4.

Abstract

To investigate the effect of Selenium Rich Yeast (SeY) on hepatotoxicity of Aluminium (Al), SeY (0.1 mg/kg) was orally administrated to aluminium-exposed mice (10 mg/kg) for 28 days. The risk of oxidative stress was assessed by detecting the total antioxidant capacity (T-AOC), catalase activity, HO content, and mRNA levels of the Keap1/Nrf-2/HO-1 pathway. Inflammatory reactions were assessed by detecting the mRNA levels of inflammatory biomarkers. Our results showed that SeY protected against the liver histological changes induce by Al. The body weight gain of mice treated with SeY + Al restore to normal compare with mice exposed to Al alone. Al treatment significantly decreased the activities of antioxidant enzymes, reduced T-AOC levels, and up-regulated the mRNA level of Nrf2 and HO-1, thereby ultimately leading to peroxidation. SeY shown a significant protective effect against oxidative stress caused by Al. In addition, Al exposure induced inflammatory responses in rat liver by promoting the release of inflammatory cytokines (TNF-a, NF-kB, TNF-R1, IL-1, IL-6, and COX-2). SeY protected against changes in liver by regulating the mRNA expression levels of inflammatory factors. These results suggested that Se protected the liver from the Al-induced hepatotoxicity by regulating the mRNA level of Keap1/Nrf2/HO-1, and inhibited inflammatory responses by down-regulating the expression level of inflammatory cytokine.

摘要

为了研究富硒酵母(SeY)对铝(Al)肝毒性的影响,将 SeY(0.1mg/kg)经口给予铝暴露的小鼠(10mg/kg)28 天。通过检测总抗氧化能力(T-AOC)、过氧化氢酶活性、HO 含量和 Keap1/Nrf-2/HO-1 途径的 mRNA 水平来评估氧化应激的风险。通过检测炎症生物标志物的 mRNA 水平来评估炎症反应。我们的结果表明,SeY 可防止 Al 引起的肝组织学变化。与单独暴露于 Al 的小鼠相比,用 SeY+Al 处理的小鼠体重增加恢复正常。Al 处理显著降低抗氧化酶的活性,降低 T-AOC 水平,并上调 Nrf2 和 HO-1 的 mRNA 水平,从而最终导致过氧化。SeY 对 Al 引起的氧化应激表现出显著的保护作用。此外,Al 暴露通过促进炎症细胞因子(TNF-a、NF-kB、TNF-R1、IL-1、IL-6 和 COX-2)的释放,在大鼠肝脏中引发炎症反应。SeY 通过调节炎症因子的 mRNA 表达水平来保护肝脏免受变化的影响。这些结果表明,Se 通过调节 Keap1/Nrf-2/HO-1 的 mRNA 水平来保护肝脏免受 Al 诱导的肝毒性,并通过下调炎症细胞因子的表达水平来抑制炎症反应。

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