Green tea increases the anti‐inflammatory tristetraprolin and decreases the pro‐inflammatory tumor necrosis factor mRNA levels in rats

• Published in: The FASEB journal 2007-04, Vol.21 (5), p.A165-A166
• Main Authors: Cao, Heping, Kelly, Meghan A., Kari, Frank, Dawson, Harry D., Coves, Sara, Roussel, Anne M., Anderson, Richard A.
• Format: Article
• Language: English
• ISSN: 0892-6638; 1530-6860
• DOI: 10.1096/fasebj.21.5.A165-d

Tristetraprolin (TTP) family proteins have anti‐inflammatory activity by binding to and destabilizing pro‐inflammatory mRNAs such as TNF mRNA, and represent a potential therapeutic target for inflammation‐related diseases. Tea has anti‐inflammatory properties but the molecular mechanism is unknown. Quantitative real‐time PCR was used to investigate the effects of green tea on the expression of TTP family genes (Zfp36/Ttp, Zfp36l1, Zfp36l2, Zfp36l3), pro‐inflammatory genes (Tnf, Gm‐csf, Cox2), and Hua, Vegfa, and Vegfb genes in rats fed a high‐fructose diet known to induce insulin resistance. TTP and ZFP36L1 mRNAs were the major forms in both liver and skeletal muscle. TTP, ZFP36L1, and ZFP36L2 mRNA levels were more abundant in the liver than muscle. GM‐CSF and ZFP36L3 mRNAs were undetectable in either tissue. Tea (1 g solid/kg diet) increased TTP mRNA levels by 50–140%, but TNF mRNA levels decreased by 30% in both tissues, and COX‐2 mRNA levels decreased by 40% in the muscle. Tea (2 g solid/kg diet) increased HuA mRNA levels by 40% in the liver, but did not affect any of the other mRNA levels in liver or muscle. These results showed that tea modulated TTP mRNA levels in rats, and that a post‐transcriptional mechanism through TTP could partially account for tea's anti‐inflammatory properties.