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Evidence-Based Complementary and Alternative Medicine
Volume 2015, Article ID 430271, 12 pages
http://dx.doi.org/10.1155/2015/430271
Research Article

Scutellarin Reduces Endothelium Dysfunction through the PKG-I Pathway

1School of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming 650500, China
2Department of Respiratory Medicine, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China
3Pharmacy Department, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China
4Department of Clinical Pharmacy, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China

Received 4 May 2015; Revised 25 July 2015; Accepted 4 August 2015

Academic Editor: Dan Hu

Copyright © 2015 Xiaohua Du et al. 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.

Abstract

Purpose. In this report, we investigated the protective mechanism of scutellarin (SCU) in vitro and in vivo which could be involved in endothelial cGMP-dependent protein kinase (PKG), vasodilator stimulated phosphoprotein (VASP) pathway, and vascular endothelium dysfunction (EtD). Method. Human brain microvascular endothelial cells (HBMECs) with hypoxia reoxygenation (HR) treatment and rats with cerebral ischemia reperfusion (CIR) treatment were applied. Protein and mRNA expression of PKG, VASP, and p-VASP were evaluated by Western blot and RT-PCR methods. Vascular EtD was assessed by using wire myography to determine endothelium-dependent vasorelaxation in isolated rat basilar artery (BA). Result. In cultured HBMECs, SCU (0.1, 1, and 10 μM) increased cell viability, mRNA, protein level, and phosphorylative activity of PKG and VASP against HR injury. In HR model of BA, SCU increased protein level of P-VASP. In rat CIR model, wire myography demonstrated that SCU (45 and 90 mg/kg, i.v.) significantly reduced ischemic size by partially restoring the endothelium dependent vasodilation of BA; PKG inhibitor Rp-8-Br-cGMPS (50 μg/kg, i.v.) reversed this protection of SCU in CIR rats. Conclusion. SCU protects against cerebral vascular EtD through endothelial PKG pathway activation.