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Oxid Med Cell Longev. 2019 Feb 25;2019:4825949. doi: 10.1155/2019/4825949. eCollection 2019.

Cherry Anthocyanins Regulate NAFLD by Promoting Autophagy Pathway.

Chu Q1,2,3, Zhang S4, Chen M1,2,3, Han W1,2,3, Jia R1,2,3, Chen W1,2,3, Zheng X1,2,3.

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Department of Food Science and Nutrition, Zhejiang University, Hangzhou 310058, China.
Zhejiang Key Laboratory for Agro-food Processing, Zhejiang University, Hangzhou 310058, China.
Fuli Institute of Food Science, Zhejiang University, Hangzhou 310058, China.
College of Environmental and Resource Science, Zhejiang University, Hangzhou 310058, China.


Nonalcoholic fatty liver disease (NAFLD) is a common chronic disease that threatens human health, and present therapies remain limited due to the lack of effective drugs. Lipid metabolic disturbance and oxidative stress have strong links to the development of NAFLD, while autophagy was generally accepted as a key regulatory mechanism on these steps. Our previous studies indicated that cherry anthocyanins (CACN) protected against high fat diet-induced obesity and NALFD in C57BL/6 mice, while the underlying molecule mechanism is still unclear. Thus, in this study, we show that CACN protect against oleic acid- (OA-) induced oxidative stress and attenuate lipid droplet accumulation in NAFLD cell models. According to the results of a transmission electron microscope (TEM), western blot, immunofluorescence (IF), and adenovirus transfection (Ad-mCherry-GFP-LC3B), autophagy is in accordance with the lipid-lowering effect induced by CACN. Further studies illustrate that CACN may activate autophagy via mTOR pathways. In addition, an autophagy inhibitor, 3-methyladenine (3-MA), was applied and the result suggested that autophagy indeed participates in the lipid clearance process in OA-induced lipid accumulation. All these results indicate that the positive effects of CACN on OA-induced hepatic lipid accumulation are mediated via activating autophagy, showing a potential target for the therapeutic strategy of NAFLD.

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