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作者

Wang, T.T. Zhou, Z.Q. Wang, S. Ji, X.W. Wu, B. Sun, L.Y. Wen, J.F. Kang, D.G. Lee, H.S. Cho, K.W. Jin, S.N.

作者单位

a School of Pharmacy, Taishan Medical University, Taian, Shandong, China Hanbang Cardio-Renal Syndrome Research Center, Wonkwang University, Iksan, Jeollabuk-do, South Korea School of Pharmacy, Ningxia Medical University, Yinchuan, Ningxia, China Institute of Cardiovascular Endocrinology, Key Laboratory of Atherosclerosis in Universities of Shandong, Taishan Medical University, Taian, Shandong, China

刊名

Journal of Physiology and Pharmacology

年份

2017

卷号

Vol.68 No.4

页码

619-628

ISSN

0867-5910

关键词

Aorta Endothelial nitric oxide synthase Euphorbia humifusa Flavonoids Guanosine 3’,5’-cyclic monophosphate Nitric oxide Phosphoinositide 3-kinase/Akt signaling pathway

摘要

Euphorbia humifusa Willd. , rich in flavonoids, has long been used for the treatment of bacillary dysentery and enteritis in China, and is known to have antioxidant, hypotensive and hypolipidemic properties. However, the vasorelaxant effect of total flavonoids of EH and action mechanisms are not clearly defined yet. The aim of the present study was to investigate the effects of TFEH on the vascular tension and its underlying mechanisms. Experiments were performed in rat thoracic aorta using the...更多

Euphorbia humifusa Willd. , rich in flavonoids, has long been used for the treatment of bacillary dysentery and enteritis in China, and is known to have antioxidant, hypotensive and hypolipidemic properties. However, the vasorelaxant effect of total flavonoids of EH and action mechanisms are not clearly defined yet. The aim of the present study was to investigate the effects of TFEH on the vascular tension and its underlying mechanisms. Experiments were performed in rat thoracic aorta using the organ bath system. TFEH caused a concentration-dependent vasorelaxation, which was dependent on a functional endothelium, and were significantly attenuated by inhibitors of endothelial NO synthase, its upstream signaling pathway, PI3K/Akt, and soluble guanylate cyclase, but not by blockade of K Ca channel, K ATP channel, cyclooxygenase, muscarinic and β-adrenergic receptors. Extracellular Ca 2+ depletion, and pre-treatment with modulators of the store-operated Ca 2+ entry channels, Gd 3+ and 2-aminoethyl diphenylborinate, significantly attenuated the TFEH-induced vasorelaxation. Our findings suggest that TFEH elicit vasorelaxation via endothelium-dependent NO-cGMP pathway through activation of PI3K/Akt- and Ca 2+ -eNOS-NO signaling. Further, it is suggested that TFEH-induced activation of the NO-soluble guanylate cyclase-cGMP-protein kinase G signaling relaxes vascular smooth muscle cells through an inhibition of the L-type Ca 2+ channel activity.收起

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