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(±)16(17)-EpDPA
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
(±)16(17)-EpDPA图片
CAS NO:155073-46-4
规格:98%
分子量:344.5
包装与价格:
包装价格(元)
25ug电议
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产品介绍
EDHF (endothelium-derived hyperpolarizing factor) is an unidentified mediator released from vascular endothelial cells in response to acetylcholine and bradykinin which is distinct from the NOS- (nitric oxide) and COX-derived (prostacyclin) vasodilators.
CAS:155073-46-4
分子式:C22H32O3
分子量:344.5
纯度:98%
存储:Store at -20°C

Background:

EDHF (endothelium-derived hyperpolarizing factor) is an unidentified mediator released from vascular endothelial cells in response to acetylcholine and bradykinin which is distinct from the NOS- (nitric oxide) and COX-derived (prostacyclin) vasodilators.[1],[2]Cytochrome P450 (CYP450) metabolism of polyunsaturated fatty acids produces epoxides such as (±)14(15)-EET which are prime candidates for the actual active mediator.[3] However, the CYP450 metabolites of eicosapentaenoic acid and docosahexaenoic acid have been little studied relative to arachidonate epoxygenase metabolites. (±)16(17)-EpDPA is the DHA homolog of (±)14(15)-EpETrE, derived via epoxidation of the 16,17-double bond of DHA. The EDHF activity of (±)16(17)-EpDPA has not yet been determined. The epoxygenase metabolites of DHA have also been detected in a mouse inflammation model.[4]


Reference:
[1]. Chataigneau, T., Félétou, M., Duhault, J., et al. Epoxyeicosatrienoic acids, potassium channel blockers, and endothelium-dependent hyperpolarization in the guinea-pig carotid artery. Br. J. Pharmacol. 123(3), 574-580 (1998).
[2]. Fisslthaler, B., Popp, R., Kiss, L., et al. Cytochrome P450 2C is an EDHF synthase in coronary arteries. Nature 401(6752), 493-497 (1999).
[3]. Baron, A., Frieden, M., and Bény, J.L. Epoxyeicosatrienoic acids activate a high-conductance, Ca2+-dependent K+ channel on pig coronary artery endothelial cells. J. Physiol. 504(Pt 3), 537-543 (1997).
[4]. Serhan, C.N., Hong, S., Gronert, K., et al. Resolvins: A family of bioactive products of ω-3 fatty acid transformation circuits by aspirin treatment that counter proinflammation signals. J. Exp. Med. 196(8), 1025-1037 (2002).