Literature DB >> 27871911

In vitro and in vivo anti-inflammatory effects of theaflavin-3,3'-digallate on lipopolysaccharide-induced inflammation.

Yanting Wu1, Fujun Jin1, Yiliang Wang2, Feng Li2, Lu Wang1, Qiaoli Wang1, Zhe Ren1, Yifei Wang3.   

Abstract

Inflammation is a defensive response against various harmful stimuli and stress conditions, such as tissue injury and one of the most common pathological processes occurring in human diseases. Theaflavin-3,3'-digallate, one of the theaflavins present in black tea, exhibits several bioactive properties, including the ability to lower the incidence of coronary heart disease, a positive effect on the bone mineral density, and the ability to prevent cancer. The aim of this study was to evaluate whether theaflavin-3,3'-digallate could reduce the production of pro-inflammatory cytokines in vivo and in vitro and ameliorate acute lung injury (ALI) in a mouse model. In this study, we demonstrated that theaflavin-3,3'-digallate suppressed the lipopolysaccharide (LPS)-induced phosphorylation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase in RAW 264.7 macrophages. In addition, we also showed that theaflavin-3,3'-digallate inhibited the expression of tumor necrosis factor alpha, interleukin -1 beta, and interleukin 6 in phorbol myristate acetate -primed U937 and RAW 264.7 cells. Furthermore, theaflavin-3,3'-digallate treatment attenuated the severity of LPS-induced ALI in mice. These results suggested that theaflavin-3,3'-digallate might be a potential therapeutic candidate for the treatment of inflammation and inflammatory diseases.
Copyright © 2016 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Acute lung injury; Inflammation; Theaflavin-3,3′-digallate Lipopolysaccharide; Theaflavins

Mesh:

Substances:

Year:  2016        PMID: 27871911     DOI: 10.1016/j.ejphar.2016.11.027

Source DB:  PubMed          Journal:  Eur J Pharmacol        ISSN: 0014-2999            Impact factor:   4.432


  15 in total

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10.  Sodium fluoride induces renal inflammatory responses by activating NF-κB signaling pathway and reducing anti-inflammatory cytokine expression in mice.

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