theaflavin-3-3--digallate and Inflammation

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.

Topics: Active Transport, Cell Nucleus; Animals; Anti-Inflammatory Agents; Biflavonoids; Catechin; Cell Line, Tumor; Cell Nucleus; Gene Expression Regulation; Humans; Inflammation; Interleukin-1beta; Interleukin-6; JNK Mitogen-Activated Protein Kinases; Lipopolysaccharides; Lung; MAP Kinase Signaling System; Mice; NF-kappa B; p38 Mitogen-Activated Protein Kinases; RAW 264.7 Cells; RNA, Messenger; Tumor Necrosis Factor-alpha