Curcumin inhibits pro‐fibrotic phenotypes in human lung fibroblasts

Abstract

Fibrosis of the lung is a common endpoint for a variety of diseases. Current available treatments have been mostly ineffective. Proliferation of pulmonary fibroblasts, enhanced production of extracellular matrix components by these cells, and differentiation of fibroblasts to myofibroblasts results in tissue fibrosis. Curcumin, a component of the widely used Ayurvedic compound turmeric, is a potent biological molecule. Numerous studies have characterized its effects on a wide variety of cellular processes and diseases. Its potential role as a therapy for pulmonary fibrosis, however, remains undefined. In this study, we show that treatment of both normal human lung fibroblasts and those obtained from patients with idiopathic interstitial pneumonias (IIPs) results in inhibition of proliferative responses and induces cell cycle arrest. In addition, curcumin inhibits transforming growth factor (TGF)‐β1‐induced myofibroblast differentiation and collagen production. The effects of curcumin were demonstrated to occur, in part, through binding and activation of the nuclear receptor, peroxisome proliferator‐activated receptor‐γ (PPAR‐γ). These observations suggest a role for curcumin as a novel agent in the treatment of fibrotic lung diseases. Supported by NIH Grants HL70068, HL57243, and PO50HL60289.