Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract only
Publication Acceptance Date: 2/12/2007
Publication Date: 3/20/2007
Citation: Cao, H., Kelly, M.A., Kari, F., Dawson, H.D., Coves, S., Roussel, A.M., Anderson, R.A. 2007. Green tea increases the antiinflammatory tristetraprolin and decreases the proinflammatory tumor necrosis factor mRNA levels in rats. [abstract]. Journal of Federation of American Societies for Experimental Biology. 21:358.4. Interpretive Summary: n/a
Technical Abstract: Tristetraprolin (TTP) family proteins have antiinflammatory activity by binding to and destabilizing proinflammatory mRNAs such as TNF mRNA, and represent a potential therapeutic target for inflammation-related diseases. Tea has antiinflammatory properties but the molecular mechanism has not been elucidated. Quantitative real-time PCR was used to investigate the effects of green tea on the expression of TTP family genes (Zfp36, Zfp36L1, Zfp36L2, Zfp36L3), proinflammatory genes (TNF, GM-CSF, COX-2), and HuR, VEGFa, and VEGFb genes in rats fed a high-fructose diet known to induce insulin resistance. TTP and Zfp36L1, and Zfp3636L2 mRNA levels were more abundant in the liver than those in the muscle. GM-CSF and Zfp36L3 mRNAs were undetectable in either tissue. Tea (1 g solid/kg diet) increased TTP mRNA level 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 HuR mRNA levels by 40% in the liver but did not affect any of the other mRNA levels in liver or muscle. These results indicate that tea could modulate TTP mRNA levels in animals and that a posttranscriptional mechanism through TTP could partially account for tea's antiinflammatory properties.