Next Article in Journal
Anti-Inflammatory Effect of 3-O-[(6'-O-Palmitoyl)-β-D-glucopyranosyl Sitosterol] from Agave angustifolia on Ear Edema in Mice
Previous Article in Journal
Cellular Transport Mechanisms of Cytotoxic Metallodrugs: An Overview beyond Cisplatin
Article Menu
Issue 10 (October) cover image

Export Article

Open AccessArticle
Molecules 2014, 19(10), 15611-15623; doi:10.3390/molecules191015611

Anti-Fibrosis Effect of Scutellarin via Inhibition of Endothelial–Mesenchymal Transition on Isoprenaline-Induced Myocardial Fibrosis in Rats

1
Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
2
Department of Cardiology, Ningbo First Hospital, Ningbo 315000, China
3
Clinical LaboratoryDepartment, Wenzhou Central Hospital, Wenzhou 325000, China
4
Coronary Care Unit, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
5
Intensive Care Unit, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
*
Author to whom correspondence should be addressed.
Received: 22 July 2014 / Revised: 14 September 2014 / Accepted: 15 September 2014 / Published: 29 September 2014
(This article belongs to the Section Medicinal Chemistry)
View Full-Text   |   Download PDF [1882 KB, uploaded 29 September 2014]   |  

Abstract

Scutellarin (SCU) is the major active component of breviscapine and has been reported to be capable of decreasing myocardial fibrosis. The aim of the present study is to investigate whether SCU treatment attenuates isoprenaline-induced myocardial fibrosis and the mechanisms of its action. Rats were injected subcutaneously with isoprenaline (Iso) to induce myocardial fibrosis and rats in the SCU treatment groups were intraperitoneally infused with SCU (10 mg·kg−1·d−1 or 20 mg·kg−1·d−1, for 14 days). Post-treatment, cardiac functional measurements and the left and right ventricular weight indices (LVWI and RVWI, respectively) were analysed. Pathological alteration, expression of type I and III collagen, Von Willebrand factor, α-smooth muscle actin, cluster of differentiation-31 (CD31), and the Notch signalling proteins (Notch1, Jagged1 and Hes1) were examined. The administration of SCU resulted in a significant improvement in cardiac function and decrease in the cardiac weight indices; reduced fibrous tissue proliferation; reduced levels of type I and III collagen; increased microvascular density; and decreased expression of α-smooth muscle actin and increased expression of CD31, Notch1, Jagged1 and Hes1 in isoprenaline-induced myocardial fibrosis in rats. Our results suggest that SCU prevents isoprenaline-induced myocardial fibrosis via inhibition of cardiac endothelial-mesenchymal transition potentially, which may be associated with the Notch pathway. View Full-Text
Keywords: scutellarin; cardiac fibrosis; EndMT; angiogenesis; notch pathway scutellarin; cardiac fibrosis; EndMT; angiogenesis; notch pathway
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Supplementary material

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Zhou, H.; Chen, X.; Chen, L.; Zhou, X.; Zheng, G.; Zhang, H.; Huang, W.; Cai, J. Anti-Fibrosis Effect of Scutellarin via Inhibition of Endothelial–Mesenchymal Transition on Isoprenaline-Induced Myocardial Fibrosis in Rats. Molecules 2014, 19, 15611-15623.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]

Molecules EISSN 1420-3049 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top