Dexamethasone and olmesartan as potential antiremodelling agents of valvular interstitial cell into myofibroblast

Rheumatic heart disease is a late complication of valvular inflammation caused by rheumatic fever. Studies have shown that the differentiation of valvular interstitial cells (VIC) into fibroblasts plays an important role in valvular remodeling and fibrosis. Various strategies to minimize valvular fibrosis has increased recently. This study aims to analyze the effect of dexamethasone, olmesartan, and its combination in inhibiting TGF-β1-induced VIC differentiation into myofibroblast. In vitro laboratory experimental-posttest only control group design was conducted. Isolated VIC of Oryctolagus cuniculus was pretreated using 2,5 ng/mL of TGF-β1 and divided into groups of dexamethasone (0.1 uM/L), olmesartan (100 nmol/L), and its combination. Inhibition of myofibroblast differentiation was quantified by the expression of α-SMA levels detected by immunofluorescence. Dexamethasone, olmesartan, and its combination administration were significantly reduced TGF-β1-induced VIC differentiation into myofibroblast expressed by α-SMA levels (dexamethasone 6823 ± 1735.3, olmesartan 6683.7 ± 2795.05). Combination of dexamethasone and olmesartan exhibit the most potent inhibition compared to control (5051.87 ± 1612.210 vs 22286.73 ± 2780.2; p < 0.000). In conclusion, dexamethasone, olmesartan, and the combination can significantly reduce the differentiation of VIC into myofibroblasts. The greatest potential is the combined effect of dexamethasone and olmesartan, while dexamethasone and olmesartan have the same potential.