comparison of the effect of epigallocatechin gallate (egcg) on α-smooth muscle actin (α-sma) expression in valve interstitial cells induced by pro-inflammatory cytokines: il-1β, il-6, tgf-β1 or tnf-α

Rheumatic heart disease (rhd) remains a persistent and widespread health concern in developing countries. fibrosis, scarring, and thickening of heart valve leaflets, commissures, and chordae tendineae are common features of rhd. valve fibrosis is characterized by the differentiation of valvular interstitial cells (vics) into myofibroblasts. these mechanisms involve pro-inflammatory cytokines, including tgf-β1, tnf-α, il-6, and il-1β. epigallocatechin gallate (egcg), a primary polyphenolic compound found in green tea, exhibits both anti-inflammatory and anti-fibrotic properties. this study aimed to evaluate the inhibitory effect of egcg on the differentiation of rabbit heart vics into myofibroblasts induced by these cytokines, based on α-sma expression. an in vitro experimental design using a post-test control group was employed. fibrosis was induced in vics isolated from new zealand rabbits (oryctolagus cuniculus) heart valves through administration of the cytokines. the interstitial cells treated with these four inducers were subsequently given egcg at 5 µm. immunocytochemical detection of α-sma served as the method to monitor the inhibition of fibroblast differentiation. the mean expression of α-sma in the treatment groups with egcg (5 µm) substantially decreased compared to each cytokine-only group. the il-6 + egcg group exhibited the lowest α-sma expression among the treatment groups. these findings suggest that egcg inhibits the differentiation of rabbit vics into myofibroblasts induced by pro-inflammatory cytokines, as indicated by reduced α-sma expression.