gallocatechin-3-gallate and Pulmonary-Fibrosis

Neutrophils play an essential role in host defense and inflammation, but the latter may trigger and sustain the pathogenesis of a range of acute and chronic diseases. Green tea has been claimed to exert anti-inflammatory properties through unknown molecular mechanisms. We have previously shown that the most abundant catechin of green tea, (-)epigallocatechin-3-gallate (EGCG), strongly inhibits neutrophil elastase. Here we show that 1) micromolar EGCG represses reactive oxygen species activity and inhibits apoptosis of activated neutrophils, and 2) dramatically inhibits chemokine-induced neutrophil chemotaxis in vitro; 3) both oral EGCG and green tea extract block neutrophil-mediated angiogenesis in vivo in an inflammatory angiogenesis model, and 4) oral administration of green tea extract enhances resolution in a pulmonary inflammation model, significantly reducing consequent fibrosis. These results provide molecular and cellular insights into the claimed beneficial properties of green tea and indicate that EGCG is a potent anti-inflammatory compound with therapeutic potential.

Topics: Administration, Oral; Angiogenesis Inhibitors; Animals; Anti-Inflammatory Agents, Non-Steroidal; Apoptosis; Catechin; Collagen; Drug Combinations; Fluorescein-5-isothiocyanate; Humans; Injections, Subcutaneous; Laminin; Mice; Mice, Inbred C57BL; Microscopy, Fluorescence; Neovascularization, Pathologic; Neutrophil Activation; Neutrophil Infiltration; Neutrophils; Oxidants; Plant Extracts; Proteoglycans; Pulmonary Fibrosis; Tea