OBJECTIVE: Tea catechins have many biological functions; these effects are induced by the suppression of several inflammatory factors. However, effects of catechins on cardiac allograft rejection have not been well investigated. METHODS AND RESULTS: To test the hypothesis that catechins can attenuate ventricular remodeling and graft arterial diseases (GAD) in cardiac rejection, we orally administered catechins to murine cardiac recipients. We analyzed the mechanisms using immunohistochemistry, RNase protection, gel mobility shift, and cell proliferation assays. Although severe myocardial cell infiltration, fibrosis, and GAD with enhancement of inflammatory factors were observed in untreated class II mismatch allografts at day 60, catechins attenuated these changes with altered Th1/Th2 cytokine balance and suppressed NF-kappaB activation and cell proliferation. CONCLUSION: Catechins are potent agents for the suppression of chronic rejection because they are critically involved in the suppression of proinflammatory signaling pathways.
OBJECTIVE:Teacatechins have many biological functions; these effects are induced by the suppression of several inflammatory factors. However, effects of catechins on cardiac allograft rejection have not been well investigated. METHODS AND RESULTS: To test the hypothesis that catechins can attenuate ventricular remodeling and graft arterial diseases (GAD) in cardiac rejection, we orally administered catechins to murine cardiac recipients. We analyzed the mechanisms using immunohistochemistry, RNase protection, gel mobility shift, and cell proliferation assays. Although severe myocardial cell infiltration, fibrosis, and GAD with enhancement of inflammatory factors were observed in untreated class II mismatch allografts at day 60, catechins attenuated these changes with altered Th1/Th2 cytokine balance and suppressed NF-kappaB activation and cell proliferation. CONCLUSION:Catechins are potent agents for the suppression of chronic rejection because they are critically involved in the suppression of proinflammatory signaling pathways.