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