Papers

Peer-reviewed
Nov, 2017

Sake lees hydrolysate protects against acetaminophen-induced hepatotoxicity via activation of the Nrf2 antioxidant pathway.

Journal of clinical biochemistry and nutrition
  • Kayoko Kawakami
  • ,
  • Chie Moritani
  • ,
  • Misugi Uraji
  • ,
  • Akiko Fujita
  • ,
  • Koji Kawakami
  • ,
  • Tadashi Hatanaka
  • ,
  • Etsuko Suzaki
  • ,
  • Seiji Tsuboi

Volume
61
Number
3
First page
203
Last page
209
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.3164/jcbn.17-21
Publisher
JOURNAL CLINICAL BIOCHEMISTRY & NUTRITION

Acetaminophen is a commonly used analgesic. However, an overdose of acetaminophen causes severe hepatotoxicity via depletion of hepatic glutathione. Here, we investigated the protective effects of sake lees hydrolysate against acetaminophen-induced hepatotoxicity in mice. Sake lees hydrolysate was administered orally to ICR mice for seven days. Six hours after acetaminophen treatment, the mice were sacrificed, and blood and liver samples were collected for analysis. Treatment with acetaminophen markedly increased the levels of serum alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase. Pretreatment with sake lees hydrolysate significantly prevented the increases in the serum levels of these enzymes and inhibited acetaminophen-mediated glutathione depletion. In addition, histopathological evaluation of the livers also revealed that sake lees hydrolysate prevented acetaminophen-induced centrilobular necrosis. The expression of γ-glutamylcysteine synthetase (γ-GCS), hemeoxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) in the liver were decreased after acetaminophen treatment, whereas pretreatment with sake lees hydrolysate led to an increased expression of all three proteins. Furthermore, sake lees hydrolysate induced the expression of these proteins in HepG2. These results suggested that sake lees hydrolysate could induces HO-1 and γ-GCS expression via activation of the Nrf2 antioxidant pathway, and protects against acetaminophen-induced hepatotoxicity in mice.

Link information
DOI
https://doi.org/10.3164/jcbn.17-21
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/29203962
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5703781
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000418634700008&DestApp=WOS_CPL
ID information
  • DOI : 10.3164/jcbn.17-21
  • ISSN : 0912-0009
  • eISSN : 1880-5086
  • Pubmed ID : 29203962
  • Pubmed Central ID : PMC5703781
  • Web of Science ID : WOS:000418634700008

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