書誌事項
- タイトル別名
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- Increased oxidative stress mediated by NOX1/NADPH oxidase promotes liver injury in a mouse model of nonalcoholic fatty liver disease
抄録
<p>A critical role of oxidative stress in the development of nonalcoholic fatty liver disease (NAFLD) has been reported. To clarify the source of oxidative stress, hepatic expression of the superoxide-generating NADPH oxidase isoforms was examined in high-fat and high-cholesterol (HFC) diet-fed mice. The level of NOX1, but not of NOX2 or NOX4 mRNA was significantly elevated in the liver of mice fed HFC diet for 8 weeks. Increased levels of serum alanine aminotransferase and hepatic cleaved caspase-3 in HFC-fed wild-type mice (WT) were significantly ameliorated in mice deficient in Nox1 (Nox1-KO). Formation of nitrotyrosine adducts, a marker of peroxynitrite-induced injury, was apparent in hepatic sinusoids of HFC diet-fed WT, which was significantly suppressed in Nox1-KO. In fact, NOX1 mRNA was predominantly expressed in the fraction of liver sinusoidal endothelial cells (LSECs). In primary cultured LSECs, palmitic acid, the most abundant saturated free fatty acid in plasma, dose-dependently up-regulated NOX1 mRNA. Accordingly, increased oxidative stress mediated by NOX1/NADPH oxidase in LSECs may promote liver injury through peroxinitrite formation in the development of NAFLD.</p>
収録刊行物
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- 日本薬理学会年会要旨集
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日本薬理学会年会要旨集 92 (0), 1-SS-53-, 2019
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390283659860643840
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- NII論文ID
- 130007812831
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- ISSN
- 24354953
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可