Abstract Title:

Extracts of bilberry (L.) fruits improve liver steatosis and injury in mice by preventing lipid accumulation and cell death.

Abstract Source:

Biosci Biotechnol Biochem. 2019 Jun 27:1-11. Epub 2019 Jun 27. PMID: 31244392

Abstract Author(s):

Sanae Haga, YiMin, Hikari Yamaki, Shigeki Jin, Tetsuya Sogon, Naoki Morita, Michitaka Ozaki

Article Affiliation:

Sanae Haga


Bilberry has been reported to have anti-oxidant and anti-inflammatory properties. We studied the effect of bilberry (L.) fruits extracts (BEs) on the pathogenesis caused by lipid accumulation in fatty liver and non-alcoholic steatohepatitis (NASH). 5μg/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 BEspossibly 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.

Study Type : Animal Study

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