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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:85.)
© 2006 American Heart Association, Inc.

Vascular Biology

Curcumin Inhibits Platelet-Derived Growth Factor–Stimulated Vascular Smooth Muscle Cell Function and Injury-Induced Neointima Formation

Xiaoping Yang; D. Paul Thomas; Xiaochun Zhang; Bruce W. Culver; Brenda M. Alexander; William J. Murdoch; Mysore N.A. Rao; David A. Tulis; Jun Ren; Nair Sreejayan

From the Division of Pharmaceutical Sciences and Center for Cardiovascular Research and Alternative Medicine (X.Y., X.Z., B.W.C., J.R., N.S.), the Division of Kinesiology and Health (D.P.T.), and the Department of Animal Sciences (B.M.A., W.J.M.), University of Wyoming, Laramie; Divis Laboratories Limited (M.N.A.R.), Hyderabad, India; and J.L. Chambers Biomedical/Biotechnology Research Institute (D.A.T.), North Carolina Central University, Durham.

Correspondence to Nair Sreejayan, Division of Pharmaceutical Sciences, School of Pharmacy, University of Wyoming, Laramie, WY 82071-3375. E-mail sreejay{at}uwyo.edu

Objective— Vascular smooth muscle cell (VSMC) migration, proliferation, and collagen synthesis are key events involved in the pathogenesis of cardiovascular disease. Growth factors, such as platelet-derived growth factor (PDGF) and fibroblast growth factor, released during vascular injury plays a pivotal role in regulating these events. Curcumin (diferuloyl methane), a major component of the spice turmeric (Curcuma longa), has been shown recently to have beneficial effects in chronic conditions, such as inflammation, cancer, cystic fibrosis, and Alzheimer’s disease. The objective of this study was to investigate the ability of curcumin to inhibit PDGF-stimulated migration, proliferation, and collagen synthesis in cultured VSMCs and neointima formation after carotid artery injury in rats.

Methods and Results— Curcumin (1 to 25 µM) produced a concentration-dependent inhibition of PDGF-elicited VSMC migration, proliferation, and collagen synthesis assessed by chemotaxis, [³H]thymidine incorporation, and [³H]-L-proline incorporation, respectively. Curcumin blocked PDGF-induced VSMC actin-cytoskeleton reorganization, attenuated PDGF signal transduction, and inhibited the binding of PDGF to its receptors. Carotid artery neointima formation was significantly attenuated by perivascular curcumin compared with vehicle controls 14 days after injury, characterized by reduced DNA synthesis, collagen synthesis, and PDGF receptor phosphorylation.

Conclusions— These data suggest that curcumin is a potent inhibitor of key PDGF-stimulated VSMC functions and may play a critical role in regulating these events after vascular injury.

Curcumin, the major component of the food additive turmeric, inhibits PDGF-stimulated smooth muscle cell proliferation, migration, and collagen synthesis. Curcumin attenuates neointima development, collagen accumulation, and upregulation of PDGF receptors in a rat arterial balloon-injury model. These effects may be attributed to the inhibition of PDGF signal transduction by curcumin.

Key Words: curcumin • neointima • platelet-derived growth factor

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