Effects Of Epigallocatechin-3-gallate On The Expression Of Inflammation-related Cytokines In Mouse Macrophage

Epigallocatechin-3-gallate (EGCG) is the most abundant and potent green tea catechin. Ithas been regarded to possess anti-cancer, antioxidant and anti-inflammation effects.Anti-inflammatory and chemopreventive activity of EGCG has attracted more and moreattention. Green tea polyphenols, and its major constituent EGCG, have been tested in tissueculture, animals and more recently in clinical trials. EGCG has been demonstrated to regulatesignal transduction pathways including: JAK/STAT, MAPK, PI3K/AKT, Wnt, Notch, NF-κBand AP-1. EGCG modulates gene expression by inhibiting various transcription factorsincluding Sp1, NF-κB, AP-1, STAT1, STAT3and FoxO1. In recent years, studies have shownthat EGCG can inhibit the expression of a variety of proinflammatory factor in macrophages.But the molecular mechanism of EGCG inflammation prevention is not entirely clear. EGCGdirectly binds to the laminin receptor (67LR) on the surface of the macrophages. Another roleof EGCG-stimulated67LR is to mediate anti-inflammatory actions in macrophages.Macrophages as an important immune cells in vivo，functional polarization has now beenobserved under inflammation conditions. In addition to producing high levels ofproinflammatory cytokines, M1macrophages also express inducible nitric oxide synthase(iNOS). However, high level of arginase-1(Arg-1) is expressed by M2macrophages. In orderto studying the effect of EGCG on macrophage phenotypes, we examined the expression ofiNOS and Arg-1in macrophages. In addition, this topic is also chosen adhesion molecule,including VCAM-1and ICAM-1, which play an important role in the inflammatory responsefor testing.We used the inflammatory model induced by LPS in mouse macrophage. Cells includingRAW264.7cell line and mouse peritoneal macrophages were used in experiments. The cellswere pretreated with EGCG (12.5μM,25μM,50μM) for2h and stimulated with LPS (1μg/ml) for24h. At the same time, control and LPS treatment were implemented. We foundthat EGCG inhibited the expression of iNOS, Arg-1, ICAM-1and VCAM-1stimulated withLPS in RAW264.7and peritoneal macrophages at the mRNA level. Effect of proinflammatoryin M1macrophages was inhibited by EGCG pretreatment. This finding further and clarify themolecular mechanism of EGCG preventing inflammation.