論文

査読有り 国際誌
2018年8月

Dimethylthiourea ameliorates carbon tetrachloride-induced acute liver injury in ovariectomized mice.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
  • Satoru Mitazaki
  • Natsumi Kotajima
  • Sakiko Matsuda
  • Naruki Ida
  • Mina Iide
  • Shigeyoshi Honma
  • Miwako Suto
  • Naho Kato
  • Naohito Kuroda
  • Kouichi Hiraiwa
  • Makoto Yoshida
  • Sumiko Abe
  • 全て表示

104
開始ページ
427
終了ページ
436
記述言語
英語
掲載種別
DOI
10.1016/j.biopha.2018.05.065

AIMS: In order to clarify hepato-protective actions of estrogen, we examined the progress of carbon tetrachloride (CCl4)-induced acute liver injury (ALI) in sham and ovariectomized (ovx) mice and the effects of dimethylthiourea (DMTU), a hydroxyl radical scavenger, and meloxicam (Melo), a selective cox-2 inhibitor, on the development of CCl4-induced ALI. MAIN METHODS: Female C57BL/6 J mice weighing 15-20 g were performed sham or ovx operation at 8 weeks of age. Blood and liver samples were collected 15 and 24 h after CCl4 administration. Sham and ovx mice were given DMTU, Melo or saline intraperitoneally 30 min before CCl4 or corn oil administration. KEY FINDINGS: ALT levels in ovx mice were significantly increased compared to those in sham mice. DMTU reduced ALT levels in ovx mice to the same levels as those in sham mice after CCl4 injection. CCl4 upregulated TNF-α, IL-6, cox-2 and iNOS expression in ovx mice compared to the levels in sham mice. DMTU significantly reduced cox-2 and iNOS expression levels upregulated by CCl4 in ovx mice. However, pretreatment with Melo had no effects on ALT levels and the gene expression levels of TNF-α, IL-6 and HO-1 in either sham or ovx mice, indicating that cox-2 may not participate in increase of CCl4-induced ALI caused by estrogen deficiency. SIGNIFICANCE: Ovariectomy accelerated the development of CCl4-induced acute liver injury, and DMTU reduced liver injury. These results suggest that estrogen may act as an antioxidant in the development CCl4-induced acute liver injury.

リンク情報
DOI
https://doi.org/10.1016/j.biopha.2018.05.065
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/29787990
ID情報
  • DOI : 10.1016/j.biopha.2018.05.065
  • ISSN : 0753-3322
  • PubMed ID : 29787990

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