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

Molecules

Hao Zhou²  Xiao Chen⁴  Lingzhi Chen⁵  Xi Zhou³  Gaoshu Zheng²  Huaiqin Zhang²  Weijian Huang²  Jiejie Cai¹ 

[1]Intensive Care Unit, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China

[2]Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China

[3] E-Mails:

[4]Coronary Care Unit, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China

[5] E-Mail:

[6]Department of Cardiology, Ningbo First Hospital, Ningbo 315000, China

[7] E-Mail:

[8]Clinical LaboratoryDepartment, Wenzhou Central Hospital, Wenzhou 325000, China

[9] E-Mail:

关键词: scutellarin;    cardiac fibrosis;    EndMT;    angiogenesis;    notch pathway;   

DOI  :  10.3390/molecules191015611

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.