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Evidence-Based Complementary and Alternative Medicine
Volume 2014 (2014), Article ID 484269, 9 pages
Research Article

Paeonol Inhibits Proliferation of Vascular Smooth Muscle Cells Stimulated by High Glucose via Ras-Raf-ERK1/2 Signaling Pathway in Coculture Model

1Key Laboratory of Xin’an Medicine, Ministry of Education, Anhui Province Key Laboratory of R&D of Chinese Medicine, Anhui University of Traditional Chinese Medicine, Hefei 230038, China
2School of Pharmacy, Anhui University of Traditional Chinese Medicine, Shihe Road 45, Hefei, Anhui 230031, China

Received 19 February 2014; Revised 29 April 2014; Accepted 18 May 2014; Published 5 June 2014

Academic Editor: Hao Xu

Copyright © 2014 Junjun Chen 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.


Paeonol (Pae) has been previously reported to protect against atherosclerosis (AS) by inhibiting vascular smooth muscle cell (VSMC) proliferation or vascular endothelial cell (VEC) injury. But studies lack how VSMCs and VECs interact when Pae plays a role. The current study was based on a coculture model of VSMCs and VECs to investigate the protective mechanisms of Pae on atherosclerosis (AS) by determining the secretory function of VECs and proliferation of VSMCs focusing on the Ras-Raf-ERK1/2 signaling pathway. VECs were stimulated by high glucose. Our data showed that high concentration (35.5 mM) of glucose induced damage in VECs. Injury of VECs stimulated VSMC proliferation in the coculture model. Pae (120 μM) decreased vascular endothelial growth factor (VEGF) and platelet derivative growth factor B (PDGF-B) release from VECs and inhibited overexpression of Ras, P-Raf, and P-ERK proteins in VSMCs. The results indicate that diabetes modulates the inflammatory response in VECs to stimulate VSMC proliferation and promote the development of AS. Pae was beneficial by inhibiting the inflammatory effects of VECs on VSMC proliferation. This study suggests the inhibitory mechanism of Pae due to the inhibition of VEGF and PDGF-B secretion in VECs and Ras-Raf-ERK1/2 signaling pathway in VSMCs.