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European Journal of Heart Failure 2007 9(2):152-159; doi:10.1016/j.ejheart.2006.05.007
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© 2007 European Society of Cardiology

Tea catechins improve left ventricular dysfunction, suppress myocardial inflammation and fibrosis, and alter cytokine expression in rat autoimmune myocarditis

Jun-ichi Suzuki*, Masahito Ogawa, Hideki Futamatsu, Hisanori Kosuge, Yuko M. Sagesaka and Mitsuaki Isobe

Department of Cardiovascular Medicine, Tokyo Medical and Dental University Tokyo 113-8519, Japan, and Central Research Institute, ITO EN, LTD., Shizuoka, Japan

* Corresponding author. Tel.: +81 03 5803 5951; fax: +81 03 5803 0133. E-mail address: jsuzuki.cvm{at}tmd.ac.jp


  Abstract

Background: Myocarditis is a clinically serious disease. Tea catechins have been shown to reduce inflammation; however the effects of catechins on the development of myocarditis have not been well studied.

Aims: To clarify the role of catechins, using an experimental autoimmune myocarditis (EAM) model.

Methods and results: Lewis rats were immunized with porcine cardiac myosin to establish EAM. Tea catechins were administered orally from day 0 to day 21 (Group A, n=12), from day 14 to day 21 (Group B, n=8), or saline (Group C, n=9) daily. Rats were killed on day 21. Echocardiograms indicated that Group A showed significantly improved cardiac function compared to Group C. Pathologically, non-treated EAM hearts showed severe myocardial cell infiltration and fibrosis; however Group A showed significantly less area. Immunohistochemistry revealed enhanced expression of NF-{kappa}B and ICAM-1 in non-treated EAM hearts, which was suppressed by catechin administration in Group A. mRNA levels of TNF-{alpha} were decreased and Th2 cytokines were markedly enhanced in Group A compared with the control group. Late catechin administration (Group B) showed limited effects on EAM.

Conclusion: The catechins suppressed ventricular remodelling in EAM; thus catechin treatment might be a promising option for the prevention of EAM myocarditis.

Key Words: Myocardial remodelling • Myocarditis • Inflammation • Echocardiogram • Cytokine • Nuclear factor

Received August 24, 2005; Revised January 13, 2006; Accepted May 11, 2006


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