Research Article Vascular Protection by Ethanol Extract of Morus alba Root Bark: Endothelium-Dependent Relaxation of Rat Aorta and Decrease of Smooth Muscle Cell Migration and Proliferation Nisha Panth , 1 Keshav Raj Paudel , 2 Dal-Seong Gong, 1 and Min-Ho Oak 1 1 College of Pharmacy and Natural Medicine Research Institute, Mokpo National University, Muan-gun, Jeonnam 58554, Republic of Korea 2 Department of Oriental Medicine Resources, Mokpo National University, Muan-gun, Jeonnam 58554, Republic of Korea Correspondence should be addressed to Min-Ho Oak; mhoak@mokpo.ac.kr Received 30 August 2018; Accepted 23 October 2018; Published 1 November 2018 Academic Editor: Stefania Marzocco Copyright © 2018 Nisha Panth et al. Tis 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. Morus alba (white mulberry) is native to the northern part of Korea and popularly used as a traditional medicine due to its numerous health benefts against human’s disease. However, the possibility that M. alba may also afect the cardiovascular system remains unexplored. Tis study sought to investigate the vascular protective efects of the root bark extract of M. alba (MAE). Vascular reactivity was performed in organ baths using isolated rat thoracic aorta, while platelet derived growth factor (PDGF) induced proliferation and migration of vascular smooth muscle cells (VSMCs) were studied by 3-(4,5-dimethylthiazol-2- yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) and wound healing assay, respectively. MAE evoked a concentration dependent vasorelaxation following endothelium-dependent pathway. However, vessel relaxations in response to MAE were markedly reduced afer endothelium removal; treatment of endothelial nitric oxide synthase inhibitor, guanylyl cyclase inhibitor, and nonspecifc potassium channel inhibitor, however, was not altered by cyclooxygenase inhibitor. Furthermore, MAE also signifcantly blunted contractile response to vasoconstrictor agent, phenylephrine. Taken together, the current evidence revealed that MAE is a potent endothelium-dependent vasodilator and this efect was involved in, at least in part, nitric oxide cyclic-guanosine monophosphate (NO-cGMP) pathway in combination with potassium (K + ) channel activation. Moreover, MAE inhibited proliferation and migration of VSMCs induced by PDGF. Terefore, MAE could be a promising candidate of natural medicine for preventing and controlling cardiovascular diseases linked with endothelial dysfunction. 1. Introduction In global scenario, cardiovascular diseases (CVDs) are still the major cause of morbidity and mortality in developed nations, while the prevalence is rising rapidly in underde- veloped country too [1, 2]. Te majority of CVDs result from complications of atherosclerosis or vascular infam- mation initiated by endothelial dysfunction and leading to various pathological conditions like peripheral arterial disease, coronary heart disease, and hypertension [3]. A single intimal layer of blood vessel composed of endothelial cell release, a potent vasodilator, and nitric oxide (NO) to maintain vascular homeostasis [4, 5]. Tis homeostasis is maintained under normal conditions by the cardioprotective role of endothelial factors. However, toxic insults to the endothelial cell by various components like oxidative stress, abnormal cholesterol level, lipid peroxidation, and mitogen lead to endothelial dysfunction that results in defect in NO production leading to impaired endothelium-dependent vasodilation [6–8]. Below the intimal endothelial cell layer, there are vascular smooth muscle cells (VSMCs) in adventitial layer. Migration of VSMCs from tunica adventitia to tunica intima followed by proliferation at that site contributes to the growth of atherosclerotic plague and restenosis [9]. Both migration and proliferation of VSMCs are initiated by num- ber of inducing factors such as platelet derived growth factors (PDGF) and tumor necrosis factor alpha (TNF-) facilitating atheroma formation in vessel wall [10]. Tese days, long- term therapeutic approach to control CVDs by treatment of modern/western medicine possesses many undesirable side Hindawi Evidence-Based Complementary and Alternative Medicine Volume 2018, Article ID 7905763, 8 pages https://doi.org/10.1155/2018/7905763