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J Agric Food Chem. 2020 Mar 4;68(9):2673-2683. doi: 10.1021/acs.jafc.0c00148. Epub 2020 Feb 25.

Theaflavin TF3 Relieves Hepatocyte Lipid Deposition through Activating an AMPK Signaling Pathway by targeting Plasma Kallikrein.

Author information

1
Tea Research Institute, Guangdong Academy of Agricultural Sciences/Guangdong Key Laboratory of Tea Resources Innovation & Utilization, Guangzhou 510640, China.
2
School of Biotechnology and Health Sciences, Wuyi University, Jiangmen 529020, P. R. China.
3
International Healthcare Innovation Institute (Jiangmen), Jiangmen 529040, P. R. China.

Abstract

Nonalcoholic fatty liver disease (NAFLD) is rapidly becoming the leading cause of chronic liver diseases throughout the world. The deficit of pharmacotherapy for NAFLD calls for an urgent need for a new drug discovery and lifestyle management. Black tea is the most popular and functional drink consumed worldwide. Its main bioactive constituent theaflavin helps to prevent obesity-a major risk factor for NAFLD. To find new targets for the development of effective and safe therapeutic drugs from natural plants for NAFLD, we found a theaflavin monomer theaflavin-3,3'-digallate (TF3), which significantly reduced lipid droplet accumulation in hepatocytes, and directly bound and inhibited the activation of plasma kallikrein (PK), which was further proved to stimulate adenosine monophosphate activated protein kinase (AMPK) and its downstream targets. Taken together, we proposed that the TF3-PK-AMPK regulatory axis is a novel mechanism of lipid deposition mitigation, and PK could be a new target for NAFLD treatment.

KEYWORDS:

AMPK kinase; black tea; hepatocyte lipid deposition; nonalcoholic fatty liver disease; plasma kallikrein; theaflavin-3,3′-digallate

PMID:
32050765
DOI:
10.1021/acs.jafc.0c00148
[Indexed for MEDLINE]

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