APCU25OS9 Comparison effect of the epigallocatechin gallate (EGCG), resveratrol, olmesartan, and atorvastatin 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
Abstract
Introduction Valve fibrosis in rheumatic heart disease (RHD) is characterized by the expression of α-smooth muscle actin (α-SMA) expression leading to its transformation into myofibroblasts. This process involves pro-inflammatory cytokines. Epigallocatechin Gallate (EGCG) exhibits anti-inflammatory and anti-fibrotic effects. Resveratrol, a compound known to have therapeutic effects on fibrosis can reduce proinflammatory responses. This study aims to demonstrate and compare the effects of EGCG, resveratrol, olmesartan, and atorvastatin in inhibiting the differentiation of rabbit heart valve interstitial cells induced by TGF-β1, TNF-α,IL-6, and IL-1β into myofibroblasts based on α-SMA expression.Methods This study is an in vitro laboratory experimental post-test only control group design. Valve interstitial cells were isolated from the heart valves of New Zealand rabbits (Oryctolagus cuniculus) and induced with fibrosis using (1) control; (2) IL-1β 10 ng/mL; (3) IL-6 50ng/mL; (4) TGF-β1 5ng/mL; and (5) TNF-α 10ng/mL. The interstitial cells treated with these four inducers were subsequently each group given EGCG 5M/L, 50µM/mL resveratrol, olmesartan 100µM/L, atorvastatin10µM/L. Fibroblast differentiation inhibition was observed with immunocytochemistry based on α-SMA expression. Comparison among the treatment groups was conducted using a one-way ANOVA with Brown-Forsythe,followed by post-hoc Bonferoni analysis for normally distributed and homogeneous data.Results A post-hoc analysis demonstrated EGCG to be the most potent compound in significantly suppressing α-SMA expression (p
Fields of Study & Subjects
Cardiac Fibrosis and Remodeling
Cardiac Valve Diseases and Treatments
Streptococcal Infections and Treatments
Publication details
- Pages
- A4.1–A4
- Publication date
- 1 February 2026
- Language
- EN