Mulberrofuran A, a New Isoprenoid 2-Arylbenzofuran from the Root Bark of the Cultivated Mulberry Tree (Morus alba L.)

Heterocycles ◽  
1978 ◽  
Vol 9 (11) ◽  
pp. 1593 ◽  
Author(s):  
Taro Nomura ◽  
Toshio Fukai ◽  
Jun Uno ◽  
Tadashi Arai
Keyword(s):  
Heterocycles ◽  
1978 ◽  
Vol 9 (6) ◽  
pp. 745 ◽  
Author(s):  
Taro Nomura ◽  
Toshio Fukai ◽  
Masa Katayanagi
Keyword(s):  

1978 ◽  
Vol 26 (5) ◽  
pp. 1394-1402 ◽  
Author(s):  
TARO NOMURA ◽  
TOSHIO FUKAI ◽  
SACHIKO YAMADA ◽  
MASA KATAYANAGI
Keyword(s):  

1976 ◽  
Vol 26 (4) ◽  
pp. 461-469 ◽  
Author(s):  
Yoshikazu YAMATAKE ◽  
Madoka SHIBATA ◽  
Masahiro NAGAI

2009 ◽  
Vol 38 (10) ◽  
pp. 1444-1451 ◽  
Author(s):  
So-Young Yoon ◽  
Jung-Soo Choi ◽  
So-Young Lee ◽  
Koth-Bong-Woo-Ri Kim ◽  
Eu-Jin Song ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Nisha Panth ◽  
Keshav Raj Paudel ◽  
Dal-Seong Gong ◽  
Min-Ho Oak

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+) channel activation. Moreover, MAE inhibited proliferation and migration of VSMCs induced by PDGF. Therefore, MAE could be a promising candidate of natural medicine for preventing and controlling cardiovascular diseases linked with endothelial dysfunction.


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