17-ODYA, a non-selective inhibitor of both ω-hydroxylation and epoxygenation of arachidonic acid via cytochrome P450 (IC50<100nM). 17-ODYA effectively suppressed the production of 20-hydroxyeicosatetraenoic acid, epoxyeicosatrienoic acids, and dihydroxyeicosatrienoic acids by rat renal cortical microsomes when exposed to arachidonic acid[1,2].
17-ODYA as the highest unique metabolite in periapical abscesses, acts an essential role in the Pathogenesis of Periapical Abscesses, one of the most frequent pathologic lesions in the alveolar bone. 17-ODYA caused significant up-regulation of interleukin-1α, interleukin-1β, interleukin-6, matrix metalloproteinase-1, monocyte chemoattractant protein-1 and platelet-derived growth factor alpha and vascular endothelial growth factor alpha at 10μmol/L in periodontal ligament fibroblasts.1μmol/L 17-ODYA caused the same effect in peripheral blood mononuclear cells. These affected cytokines have important biological activities in coordinating the body's response to infection[3].
17-ODYA delivered via the superfusate for 45mins at 10mmol/l, inhibits both local and conducted responses of microiontophoresis of ACh evoked vasodilation that conducted along arterioles in C57Bl6 mice[4].
References:
[1] Zou A P, Ma Y H, Sui Z H, et al. Effects of 17-octadecynoic acid, a suicide-substrate inhibitor of cytochrome P450 fatty acid omega-hydroxylase, on renal function in rats[J]. Journal of Pharmacology and Experimental Therapeutics, 1994, 268(1): 474-481.
[2] Manicam C, Ginter N, Li H, et al. Compensatory vasodilator mechanisms in the ophthalmic artery of endothelial nitric oxide synthase gene knockout mice[J]. Scientific reports, 2017, 7(1): 7111.
[3] Altaie A M, Mohammad M G, Madkour M I, et al. The essential role of 17-octadecynoic acid in the pathogenesis of periapical abscesses[J]. Journal of Endodontics, 2023, 49(2): 169-177. e3.
[4] Hnngerford J E, Sessa W C, Segal S S. Vasomotor control in arterioles of the mouse cremaster muscle[J]. The FASEB journal, 2000, 14(1): 197-207.
17-ODYA是一种非选择性抑制剂，通过细胞色素P450抑制花生四烯酸的ω-羟基化和环氧化作用（IC50<100nM）。当花生四烯酸暴露于大鼠肾皮质微粒体时，17-ODYA有效地抑制了20-羟基二十碳四烯酸、环氧二十碳三烯酸和二羟基二十碳三烯酸的产生[1,2]。
17-ODYA 是根尖周脓肿中含量最高的独特代谢物，在根尖周脓肿的发病机制中起着至关重要的作用，根尖周脓肿是牙槽骨中最常见的病变之一。 在牙周韧带成纤维细胞中，当浓度为 10μmol/L 时，17-ODYA 会显著上调 白介素-1α、白介素-1β、白介素-6、基质金属蛋白酶-1、单核细胞趋化蛋白-1、血小板衍生生长因子α和血管内皮生长因子α。这些细胞因子在协调机体对感染的反应方面具有重要的生物活性[3]。
17-ODYA以10mmol/L的浓度经由超滤液注入，连续注入45分钟，可以抑制C57Bl6小鼠沿动脉小分支传导的乙酰胆碱诱导的血管舒张的局部和传导性反应[4]。