抄録
Chronic pancreatitis is histopathologically characterized by the progression of pancreatic fibrosis. Pancreatic stellate cells (PSCs) play a principal role in the development of pancreatic fibrosis. Tranilast suppresses collagen synthesis of fibroblasts derived from keloid hypertrophic scars and cell proliferation of fibroblasts. Hence, we hypothesize that tranilast suppresses fibrosis and is effective against pancreatic fibrosis. In this study, we examined the effect of tranilast on cell proliferation, activation, and collagen synthesis of cultured PSCs. Tranilast significantly inhibited the proliferation of PSCs when they were cultured with and without of platelet-derived growth factor (PDGF) and decreased the expression of alpha smooth muscle actin (α-SMA) in cultures with Transforming Growth Factor-β1 (TGF-β1) and PDGF. Tranilast did not cause a significant dose-dependent reduction in the amount of collagen in the medium. Neither did it significantly affect the expression of Col-1 mRNA compared to the control. Our results suggest that tranilast inhibits the development of pancreatic fibrosis, making it a potential therapeutic agents for chronic pancreatitis.
