Curcumin Suppress Cardiac Fibroblasts Activities by Regulating Proliferation, Migration, and the Extracellular Matrix

Cardiac fibrosis plays a critical role in the pathophysiology of cardiovascular disease. It has been observed that curcumin has several cardiovascular effects. The purpose of this study was to evaluate whether curcumin can attenuate cardiac fibroblasts activity.

We evaluated the migration, proliferation, collagen production, and transcription signaling in rat cardiac fibroblasts isolated from Sprague-Dawley rats (males, weighing 300-350 g) that were or were not incubated with curcumin (25 μM) and the co-administration of transforming growth factor (TGF)- β1 (10 ng/ml) or angiotensin (Ang) II (100 nM) by a cell migration analysis, proliferation assay, and Western blot analysis. Compared to those without curcumin, curcumin-treated cardiac fibroblasts exhibited lower migratory, proliferative abilities and collagen production at the baseline and after the co-administration of TGF-β1 or Ang II. Curcumin-treated cardiac fibroblasts had increased matrix metalloproteinase (MMP)-2 activity in the presence of Ang II treatment. Curcumin-treated cardiac fibroblasts down-regulated phosphorylated protein kinase B (Akt) and phosphorylated Smad2/3 expression irrespective of TGF-β1 treatment. Curcumin also decreased phosphorylated extracellular signal-regulated kinase (ERK)1/2 levels in the presence of Ang II.

Curcumin attenuated Akt, Smad2/3, and ERK1/2 phosphorylation which were mediated by TGF-β1 and angiotensin II. This resulted in decreased cardiac fibroblast activation and supports the assertion that curcumin is an effective antifibrotic agent which can be used to treat heart failure.

Angiotensin; Curcumin; Fibroblasts; Heart failure; Transforming growth factor.