論文

査読有り
2017年11月

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

61
3
開始ページ
203
終了ページ
209
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3164/jcbn.17-21
出版者・発行元
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.

Web of Science ® 被引用回数 : 2

リンク情報
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

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