Journal
FRONTIERS IN PHARMACOLOGY
Volume 9, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2018.00653
Keywords
polyphenols; 4-hydroxyphenylacetic acid 4-HPA; acetaminophen APAP; hepatotoxicity; oxidative stress; nuclear factor erythroid 2-related factor; Nrf2
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Funding
- National Key Research and Development Program of China [2017YFD0501400]
- SCO Regional collaborative innovation project, Xinjiang [2016E03012]
- Key Construction Program of International Cooperation Base in S&T, Shaanxi Province [2015SD0018]
- Program for Science & Technology Innovation Talents in Universities of Henan Province - national funds through the FCT I.P. [18HASTIT035, UID/BIA/04050/2013 (POCI-01-0145-FEDER-007569)]
- Ministerio da Ciencia, Tecnologia e Ensino Superior (MCTES)
- ERDF through the COMPETE2020 - Programa Operacional Competitividade e Internacionalizacao (POCI), Portugal
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Acetaminophen (APAP) overdose is the principal cause of drug-induced acute liver failure. 4-hydroxyphenylacetic acid (4-HPA), a major microbiota-derived metabolite of polyphenols, is involved in the antioxidative action. This study seeks to investigate the ability of 4-HPA to protect against APAP-induced hepatotoxicity, as well as the putative mechanisms involved. Mice were treated with 4-HPA (6, 12, or 25 mg/kg) for 3 days, 1 h after the last administration of 4-HPA, a single dose of APAP was intraperitoneally infused for mice. APAP caused a remarkable increase of oxidative stress markers, peroxynitrite formation, and fewer activated phase II enzymes. 4-HPA increased Nrf2 translocation to the nucleus and enhanced the activity of phase II and antioxidant enzymes, and could thereby ameliorate APAP-induced liver injury. Studies reveal that 4-HPA, as an active area of bioactive dietary constituents, could protect the liver against APAP-induced injury, implying that 4-HPA could be a new promising strategy and natural hepatoprotective drug.
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