First Author | Yang F | Year | 1998 |
Journal | J Nutr | Volume | 128 |
Issue | 12 | Pages | 2334-40 |
PubMed ID | 9868178 | Mgi Jnum | J:51543 |
Mgi Id | MGI:1316887 | Doi | 10.1093/jn/128.12.2334 |
Citation | Yang F, et al. (1998) Green tea polyphenols block endotoxin-induced tumor necrosis factor- production and lethality in a murine model. J Nutr 128(12):2334-40 |
abstractText | Green tea polyphenols are potent antioxidants. They have both anti- cancer and anti-inflammatory effects. However, their mechanisms of actions remain unclear. In inflammation, tumor necrosis factor- alpha(TNFalpha) plays a pivotal role. NF-KB, an oxidative stress - sensitive nuclear transcription factor, controls the expression of many genes including the TNFalpha gene. We postulated that green tea polyphenols regulate TNFalpha gene expression by modulating NF-KB activation through their antioxidant properties. In the macrophage cell line, RAW264.7, (-)epigallocatechin gallate (EGCG), the major green tea polyphenol, decreased lipopolysaccharide (LPS)-induced TNFalpha production in a dose-dependent fashion (50% inhibition at 100 mmol/L). EGCG also inhibited LPS-induced TNFalpha mRNA expression and nuclear NF- KB-binding activity in RAW264.7 cells (30-40% inhibition at 100 mmol/L). Similarly, EGCG inhibited LPS-induced TNFalpha production in elicited mouse peritoneal macrophages. In male BALB/c mice, green tea polyphenols (given by oral gavage 2 h prior to an i.p. injection of 40 mg LPS/kg body wt) decreased LPS-induced TNFalpha production in serum in a dose-responsive fashion. At a dose of 0.5 g green tea polyphenols/kg body wt, serum TNFalpha was reduced by 80% of control. Moreover, 0.5 g green tea polyphenols/kg body wt completely inhibited LPS-induced lethality in male BALB/c mice. We conclude that the anti- inflammatory mechanism of green tea polyphenols is mediated at least in part through down-regulation of TNFalpha gene expression by blocking NF- KB activation. These findings suggest that green tea polyphenols may be effective therapy for a variety of inflammatory processes. |