Tranilast attenuates vascular hypertrophy, matrix accumulation and growth factor overexpression in experimental diabetes

Abstract

Objectives: The growth factors transforming growth factor-β (TGF-β) and epidermal growth factor (EGF) have both been implicated in the hypertrophic structural changes in the vasculature that are characteristic features of both human and experimental diabetes. Recently, tranilast (N(3,4-dimethoxycinnamoyl)anthranilic acid), a drug used in the treatment of allergic and dermatological diseases, has also been reported to inhibit transforming growth factor-β (TGF-β)-mediated collagen formation. However, its effects on vascular hypertrophy in diabetes are unknown. The present study thus sought to determine the effects of tranilast on both TGF-β and EGF expression and mast cells in mediating the tr..