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首页> 外文期刊>Biochemical Pharmacology >Acetaminophen-induced liver injury is attenuated in transgenic fat-1 mice endogenously synthesizing long-chain n-3 fatty acids
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Acetaminophen-induced liver injury is attenuated in transgenic fat-1 mice endogenously synthesizing long-chain n-3 fatty acids

机译：乙酰氨基酚诱导的肝损伤在内源合成长链N-3脂肪酸的转基因脂肪-1小鼠中衰减

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摘要

Acetaminophen (APAP) overdose-induced hepatotoxicity is the most commonly cause of drug-induced liver failure characterized by oxidative stress, mitochondrial dysfunction, and cell damage. Therapeutic efficacy of omega-3 polyunsaturated fatty acids (n-3 PUFA) in several models of liver disease is well documented. However, the impacts of n-3 PUFA on APAP hepatotoxicity are not adequately addressed. In this study, the fat-1 transgenic mice that synthesize endogenous n-3 PUFA and wild type (WT) littermates were injected intraperitoneally with APAP at the dose of 400 mg/kg to induce liver injury, and euthanized at 0h, 2h, 4h and 6h post APAP injection for sampling. APAP overdose caused severe liver injury in WT mice as indicated by serum parameters, histopathological changes and hepatocyte apoptosis, which were remarkably ameliorated in fat-1 mice. These pro tective effects of n-3 PUFA were associated with regulation of the prolonged JNK activation via inhibition of apoptosis signal-regulating kinase 1 (ASKl)/mitogen-activated protein kinase kinase 4 (MKK4) pathway. Additionally, the augment of endogenous n-3 PUFA reduced nuclear factor kappa B (NF-kB) - mediated in flammation response induced by APAP treatment in the liver. These findings indicate that n-3 PUFA has potent protective effects against APAP-induced acute liver injury, suggesting that n-3 dietary supplement with n-3 PUFA may be a potential therapeutic strategy for the treatment of hepatotoxicity induced by APAP overdose.
机译：乙酰氨基酚（APAP）过量诱导的肝毒性是药物诱导的药物诱导肝功能障碍的最常见原因，其特征在于氧化应激，线粒体功能障碍和细胞损伤。 ω-3多不饱和脂肪酸（N-3 PUFA）在几种肝脏疾病模型中的治疗疗效得到了很好的记录。然而，N-3 PUFA对APAP肝毒性的影响没有充分解决。在该研究中，用400mg / kg的剂量腹腔内腹膜内注射脂肪-1转基因小鼠，以400mg / kg诱导肝损伤，并在0h，2h，4h中安乐死和6H后Apap注入采样。 APAP过量导致WT小鼠的严重肝损伤，如血清参数，组织病理学变化和肝细胞凋亡所述，其在脂肪-1小鼠中显着改善。通过抑制凋亡信号调节激酶1（Ask1）/丝裂剂活化的蛋白激酶激酶4（MKK4）途径，N-3 PUFA的这些PRO调节与延长的JNK活化的调节有关。另外，增强内源性N-3 PUFA减少的核因子Kappa B（NF-KB） - 在肝脏中APAP治疗诱导的烧结反应中介导。这些发现表明，N-3 PUFA对APAP诱导的急性肝损伤具有有效的保护作用，表明N-3与N-3 PUFA的膳食补充剂可以是治疗通过APAP过量诱导的肝毒性的潜在治疗策略。

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  • 来源
    《Biochemical Pharmacology》 |2018年第2018期|共14页
  • 作者

    Feng Ruibing; Wang Yang; Liu Conghui; Yan Chunyan; Zhang Hang; Su Huanxing; Kang Jing X.; Shang Chang-Zhen; Wan Jim-Bo;

  • 作者单位

    Univ Macau Inst Chinese Med Sci State Key Lab Qual Res Chinese Med Macau Peoples R China;

    Univ Macau Inst Chinese Med Sci State Key Lab Qual Res Chinese Med Macau Peoples R China;

    Univ Macau Inst Chinese Med Sci State Key Lab Qual Res Chinese Med Macau Peoples R China;

    Guangdong Pharmaceut Univ Coll Pharm Guangzhou Guangdong Peoples R China;

    Guangdong Pharmaceut Univ Coll Pharm Guangzhou Guangdong Peoples R China;

    Univ Macau Inst Chinese Med Sci State Key Lab Qual Res Chinese Med Macau Peoples R China;

    Massachusetts Gen Hosp LLMT Boston MA 02114 USA;

    Sun Yat Sen Univ Sun Yat Sen Mem Hosp Dept Hepatopancreatobiliary Surg Guangzhou Guangdong;

    Univ Macau Inst Chinese Med Sci State Key Lab Qual Res Chinese Med Macau Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 药理学;
  • 关键词

    Acetaminophen; N-3 polyunsaturated fatty acids; Hepatotoxicity; JNK; Inflammatory;

    机译：乙酰氨基酚;N-3多不饱和脂肪酸;肝毒性;JNK;炎症;

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