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- Title
Extracts of bilberry (Vaccinium myrtillus L.) fruits improve liver steatosis and injury in mice by preventing lipid accumulation and cell death.
- Authors
Haga, Sanae; YiMin; Yamaki, Hikari; Jin, Shigeki; Sogon, Tetsuya; Morita, Naoki; Ozaki, Michitaka
- Abstract
Bilberry has been reported to have anti-oxidant and anti-inflammatory properties. We studied the effect of bilberry (Vaccinium myrtillus L.) fruits extracts (BEs) on the pathogenesis caused by lipid accumulation in fatty liver and non-alcoholic steatohepatitis (NASH). 5 μg/ml of BEs was enough to suppress lipid accumulation in the fatty liver model of the mouse hepatic AML12 cells. BEs increased cell viability and anti-oxidant capacity, presumably by activating (phosphorylating) Akt/STAT3 and inducing MnSOD/catalase. BEs also significantly reduced Rubicon and induced p62/SQSTM1, possibly contributing to reduce cellular lipids (lipophagy). When the mice were fed supplemented with BEs (5% or 10%, w/w), hepatic steatosis, injury, and hypercholesterolemia/hyperglycemia were significantly improved. Furthermore, histological and cytokine studies indicated that BEs possibly suppress hepatic inflammation (hepatitis) and fibrosis. Therefore, BEs improved liver steatosis and injury, and potentially suppress fibrosis by suppressing inflammatory response, which therefore may prevent the progression of fatty liver to NASH. Bilberry fruits extracts suppressed hepatocyte injury caused by early fat accumulation. Therefore, bilberry is expected to be a liver-friendly food.
- Subjects
BILBERRY; LIVER injuries; CELL death; FRUIT; FATTY liver; NON-alcoholic beverages
- Publication
Bioscience, Biotechnology & Biochemistry, 2019, Vol 83, Issue 11, p2110
- ISSN
0916-8451
- Publication type
Article
- DOI
10.1080/09168451.2019.1634514