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Sulforaphane prevents acetaminophen-induced hepatic injury in mice.

机译：萝卜硫烷可预防对乙酰氨基酚引起的小鼠肝损伤。

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摘要

Sulforaphane (SFN), an isothiocyanate found in cruciferous vegetables, is known to confer antioxidant protection in vivo. Rather than directly reacting with free radicals, however, SFN works by inducing Nrf2, a transcription factor that binds to the promoter regions of several known antioxidant genes and enhances detoxification. Because oxidative stress is a major contributor to acetaminophen (APAP)-induced hepatotoxicity, SFN may defend the liver against APAP overdose by activating the Nrf2 pathway and increasing endogenous antioxidant response. To test this hypothesis, mice were pre-treated with SFN for four days, injected with APAP on the fifth day, and sacrificed shortly thereafter. APAP overdose caused massive hepatic injury, as shown by increases in serum liver enzyme activity and lipid peroxidation. APAP overdose also manifested as decreases in total glutathione and glutathione reductase activity. SFN administration clearly prevented these manifestations of liver injury, however: increases in serum liver enzyme activity and lipid peroxidation were blunted, while total glutathione and glutathione reductase activity remained similar to those of control animals. SFN treatment did not affect the catalytic activity of acetaminophen-metabolizing enzyme CYP2E1, but did increase nuclear accumulation of Nrf2, suggesting that SFN acts primarily through the Nrf2 pathway. In summary, these data support the hypothesis that sulforaphane attenuates acute acetaminophen-induced liver injury. This decrease in injury results from the increased availability of glutathione to react with toxic metabolites of acetaminophen.
机译：十字花科蔬菜中发现的异硫氰酸酯萝卜硫素（SFN）可在体内提供抗氧化保护。但是，SFN不是直接与自由基反应，而是通过诱导Nrf2起作用，Nrf2是一种转录因子，可与几种已知的抗氧化剂基因的启动子区域结合并增强解毒作用。因为氧化应激是对乙酰氨基酚（APAP）诱导的肝毒性的主要贡献者，所以SFN可能通过激活Nrf2途径和增加内源性抗氧化剂反应来保护肝脏免于APAP过量。为了检验该假设，将小鼠用SFN预处理四天，在第五天注射APAP，然后不久将其处死。过量服用APAP会造成严重的肝损伤，如血清肝酶活性和脂质过氧化作用的增加所表明。 APAP过量也表现为总谷胱甘肽和谷胱甘肽还原酶活性降低。 SFN给药明显预防了肝损伤的这些表现，但是：血清肝酶活性和脂质过氧化作用增加了，而总谷胱甘肽和谷胱甘肽还原酶活性仍然与对照动物相似。 SFN处理不会影响对乙酰氨基酚代谢酶CYP2E1的催化活性，但会增加Nrf2的核积累，表明SFN主要通过Nrf2途径起作用。总而言之，这些数据支持了萝卜硫烷减轻急性对乙酰氨基酚引起的肝损伤的假设。伤害的减少是由于谷胱甘肽与对乙酰氨基酚的有毒代谢物发生反应的可能性增加。

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  • 作者

    Schmidt, Robin H.;

  • 作者单位

    University of Louisville.;

  • 授予单位 University of Louisville.;
  • 学科 Health Sciences Toxicology.;Health Sciences Pharmacology.
  • 学位 M.S.
  • 年度 2011
  • 页码 25 p.
  • 总页数 25
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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