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Title: Green tea polyphenols avert chronic inflammation-induced myocardial fibrosis of female rats

Author
item SHEN, CHWAN-LI - Texas Tech University
item SAMATHANAM, CHRISTINA - Texas Tech University
item TATUM, OWATHA - Texas Tech University
item GRAHAM, SUZANNE - Texas Tech University
item TUBB, CHRISTINE - Texas Tech University
item Cao, Jay
item DUNN, DALE - Texas Tech University
item WANG, JIA-SHENG - University Of Georgia

Submitted to: Inflammation Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/11/2011
Publication Date: 3/4/2011
Citation: Shen, C., Samathanam, C., Tatum, O.L., Graham, S., Tubb, C., Cao, J.J., Dunn, D.M., Wang, J. 2011. Green tea polyphenols avert chronic inflammation-induced myocardial fibrosis of female rats. Inflammation Research. 60(7):665-672.

Interpretive Summary: The pathogenesis of atherosclerosis is strongly associated with chronic inflammation. Green tea polyphenols possess anti-oxidant and/or anti-inflammatory property and may have beneficial effects on the prevention of cardiovascular diseases. In present study, we evaluated whether green tea polyphenols (green tea bioactive components) can prevent myocardial fibrosis in female with chronic inflammation induced by lipopolysaccharide implantation. We found that lipopolysaccharide implantation increased myocardial fibrosis in coronary vessels and surrounding myocardium. Supplementation of green tea polyphenols reversed lipopolysaccharide-induced detrimental changes. After 4 wk supplementation, green tea polyphenols decreased white blood cell counts, lymphocytes, neutrophils and eosinophils. We conclude that green tea polyphenols have a protective role in chronic inflammation-induced myocardial fibrosis.

Technical Abstract: Objective: Green tea proposes anti-inflammatory properties which may attenuate chronic inflammation-induced fibrosis of vessels. This study evaluated whether green tea polyphenols (GTP) can avert fibrosis or vascular disruption along with mechanisms in rats with chronic inflammation. Treatments: Forty 3-month-old female rats were assigned to a 2 (placebo vs. lipopolysaccharide, administration) x 2 (no GTP vs. 0.5% GTP in drinking water) factorial design for 12 weeks. Methods: Masson’s trichrome staining evaluated myocardial fibrosis in coronary vessels and surrounding myocardium. Whole blood specimens were counted for differentials. Spleen TNF-alpha mRNA expression was determined by real-time RT-PCR. Data were analyzed by two-way ANOVA followed by mean separation procedures. Results: After 12 weeks, lipopolysaccharide administration induced myocardial fibrosis in vessels and surrounding myocardium, spleen TNF-alpha mRNA expression, and leukocytes, while GTP supplementation in drinking water significantly averted such observation. Conclusions: GTP attenuates myocardial fibrosis through a suppression of chronic inflammation and innate immune responses.