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Oroxylin A can induce the relaxation of the aorta ring in endothelium-dependent manner. Nitric oxide may be involved in the endothelium-dependent effect of oroxylin A.

1) These compounds might contribute to the anti-hypertensive effect collectively. However, the anti-hypertensive effect of Eucommia ulmoides OLIV. bark remains largely unclear.Pharmacological studies have revealed that Eucommia ulmoides OLIV. bark extract induce endothelium and NO-cyclic guanosine monophosphate (cGMP) dependent relaxation in the rat thoracic aorta.2) Another report demonstrated that the endothelium-dependent vascular relaxation induced by the bark extract is mediated by NO and endothelium-derived hyperpolarizing factor in small vessels.3) However, the vasorelaxing components have been unclear. Recently, we found oroxylin A and wogonin isolated from Eucommia ulmoides OLIV. bark could significantly lower the perfusion pressure.4) In the previous study, we had reported that oroxylin A could relax rat thoracic aorta and it was endothelium and NO dependent.5)The present study was undertaken to investigate vasodilatory effect of wogonin and its mechanism.Wogonin ( Fig. 1) is a flavone and has a variety of cardiovascular protective effect. It could regulate migration, proliferation and apoptosis of vascular smooth muscle cells. [6][7][8] Besides, wogonin could inhibit angiogenesis, suppress collagen deposition in cardiac fibroblasts and inhibit ischemic brain injury. [9][10][11][12] There is no evidence for vascular relaxation effect of wogonin. We describe here that wogonin, unlike oroxylin A, is an endothelium-and NO-independent vasodilatory flavonoid. One report demonstrated that wogonin offered a wide margin of safety.13) It has therapeutic potential for the treatment of cardiovascular and cerebrovascular diseases.

Oroxylin A, a flavonoid, is naturally produced in many medicinal plants. Our previous study identified it as a phytoestrogen. Based on this, the present study investigated its vasoconstriction reducing effects and whether the action was mediated by the estrogen receptor (ER) signal pathway. Long-term in vitro treatment with oroxylin A reduced Ach-induced vasorelaxation and NE-mediated or KCl-mediated contractile responses in rat aortic rings. These effects were interfered by an ER inhibitor ICI 182,780. Rat cardiac microvascular endothelial cells (CMECs) and aortic vascular smooth muscle cells (VSMCs) were used to study the possible underlying mechanisms. Oroxylin A activated the ER signal pathway. In CMECs, it increased NO production and eNOS protein expression. In VSMCs, it promoted NO production and iNOS protein expression. These effects were also inhibited by ICI 182,780. Besides, oroxylin A stimulated ERα and ERβ protein expression in CMECs and VSMCs. All these findings suggest that the ER signal pathway takes part in the vasoconstriction reducing effects of oroxylin A.