Affect of Aramchol on TGFβ stimulated H69 Cholangiocytes

Cholestatic liver diseases, such as primary sclerosing cholangitis (PSC), are characterized by biliary fibroinflammation. Transforming growth factor-β (TGFβ) activated cholangiocytes release signals that recruit immune cells to drive inflammation and activate myofibroblasts to deposit the extracellular matrix (ECM). TGFβ regulates stearoyl-CoA desaturase (SCD) in stimulating lipid signaling. However, the role of SCD or its inhibitor, Aramchol, has not been investigated in biliary fibroinflammation. Here we used human transformed H69 cholangiocytes that were treated with TGFβ (10ng/mL) with and without Aramchol acid (30µM) overnight. RNA-seq analysis showed significant inhibition of TGFβ-induced hepatic fibrosis pathways while upregulating peroxisome proliferator-activated receptor (PPAR) signaling by Aramchol. RNA-seq profiling of human H69 cholangiocytes stimulated with TGFβ (10ng/mL) with and without Aramchol acid (30uM) overnight.