首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >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
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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

机译:桑树根皮乙醇提取物的血管保护作用:大鼠主动脉内皮依赖性舒张和平滑肌细胞迁移和增殖的减少

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Morus alba (white mulberry) is native to the northern part of Korea and popularly used as a traditional medicine due to its numerous health benefits against human’s disease. However, the possibility that M. alba may also affect the cardiovascular system remains unexplored. This study sought to investigate the vascular protective effects 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 after endothelium removal; treatment of endothelial nitric oxide synthase inhibitor, guanylyl cyclase inhibitor, and nonspecific potassium channel inhibitor, however, was not altered by cyclooxygenase inhibitor. Furthermore, MAE also significantly blunted contractile response to vasoconstrictor agent, phenylephrine. Taken together, the current evidence revealed that MAE is a potent endothelium-dependent vasodilator and this effect was involved in, at least in part, nitric oxide cyclic-guanosine monophosphate (NO-cGMP) pathway in combination with potassium (K
机译:Morus alba(桑)原产于韩国北部,由于其对人类疾病的众多健康益处,因此被广泛用作传统药物。但是,白念珠菌也可能影响心血管系统的可能性尚未得到探讨。这项研究旨在调查白僵菌(MAE)根皮提取物的血管保护作用。使用分离的大鼠胸主动脉在器官浴中进行血管反应,同时通过3-(4,5-二甲基噻唑-2-基)-研究血小板衍生生长因子(PDGF)诱导的血管平滑肌细胞(VSMC)增殖和迁移。 5-(3-羧基甲氧基苯基)-2-(4-磺基苯基)-2H-四唑鎓(MTS)和伤口愈合试验。 MAE在内皮依赖性途径后诱发了浓度依赖性血管舒张。然而,去除内皮后,对MAE的血管舒张作用明显降低。内皮一氧化氮合酶抑制剂,鸟苷酰环化酶抑制剂和非特异性钾通道抑制剂的治疗方法,并没有被环氧合酶抑制剂改变。此外,MAE还显着减弱了对血管收缩药苯肾上腺素的收缩反应。综上所述,目前的证据表明,MAE是一种有效的内皮依赖性血管舒张剂,这种作用至少部分参与了一氧化氮环鸟苷单磷酸(NO-cGMP)途径与钾(K

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