Glaucocalyxin A attenuates angiotensin II-induced cardiac fibrosis in cardiac fibroblasts
- Department of Emergency, Huaihe Hospital, Henan University, Kaifeng, 475000 (China)
- Department of Cardiology, Huaihe Hospital, Henan University, Kaifeng, 475000 (China)
Highlights: • GLA inhibits Ang II-induced proliferation and migration of CFs. • GLA prevents the differentiation of CFs to myofibroblasts. • GLA inhibits the production of ECM and MMPs in Ang II-stimulated CFs. • GLA prevents TGF-β1/Smad3 pathway activation induced by Ang II in CFs. Glaucocalyxin A (GLA) is a natural ent-Kaurane diterpenoid that possesses cardioprotective effect. Recently, it has been reported that GLA inhibits liver and pulmonary fibrosis, whereas its role in cardiac fibrosis remains unknown. In the present study, we evaluated the effect of GLA on the pathogenesis of cardiac fibrosis in vitro. The results showed that GLA inhibited angiotensin II (Ang II)-induced proliferation and migration in cardiac fibroblasts (CFs). GLA reduced the expression of alpha-smooth muscle actin (α-SMA) in Ang II-induced CFs, suggesting that GLA prevented the differentiation of CFs to myofibroblasts. Furthermore, the production of extracellular matrix (ECM) components including type I collagen (Col-I) and fibronectin, as well as the matrix metalloproteinases (MMPs) including MMP-2 and MMP-9 were reduced by GLA in Ang II-induced CFs. In addition, GLA prevented the Ang II-induced activation of transforming growth factor beta 1 (TGF-β1)/Smad3 pathway in CFs. Collectively, our results demonstrated that GLA acted as an anti-fibrotic agent in cardiac fibrosis, which might be mediated by the regulation of TGF-β1/Smad3 pathway. GLA might be an attractive candidate for improving the prognosis of acute myocardial infarction (AMI) by controlling the cardiac fibrosis.
- OSTI ID:
- 23134332
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 503, Issue 3; Other Information: Copyright (c) 2018 Published by Elsevier Inc.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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