全氟羧酸比 12-脂氧合酶途径更能抑制大鼠血小板中环氧化酶途径。
Perfluorinated carboxylic acids inhibit cyclooxygenase pathway more potently than 12-lipoxygenase pathway in rat platelets.
机构信息
Laboratory of Physiological Chemistry, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan.
出版信息
Prostaglandins Leukot Essent Fatty Acids. 2010 Oct-Dec;83(4-6):225-8. doi: 10.1016/j.plefa.2010.07.003. Epub 2010 Aug 3.
Two perfluorinated carboxylic acids (PFCAs), pentadecafluorooctanoic acid (PDFOA) and heptadecafluorononanoic acid (HDFNA), were investigated for potential modulatory effects on the cyclooxygenase (COX) and 12-lipoxygenase (LOX) metabolisms in rat platelets. Both PDFOA and HDFNA dose-dependently inhibited the formation of a COX metabolite, 12-HHT, without any effect on that of a LOX metabolite, 12-HETE, at concentrations ranging from 10 to 100μM. These two PFCAs up to 100μM did not affect platelet membrane integrity, and COX-1 and -2 protein expression levels in Caco-2 cells. These results suggest that PDFOA and HDFNA have the potential to modify platelet function by inhibiting the COX pathway at activity level, but not at protein level.
两种全氟羧酸（PFCAs），十五氟辛酸（PDFOA）和十七氟壬酸（HDFNA），被研究用于调节大鼠血小板中环氧化酶（COX）和 12-脂氧合酶（LOX）代谢的潜在作用。在 10 到 100μM 的浓度范围内，PDFOA 和 HDFNA 均呈剂量依赖性地抑制 COX 代谢物 12-HHT 的形成，而对 LOX 代谢物 12-HETE 没有任何影响。这两种 PFCAs 即使在高达 100μM 的浓度下，也不会影响血小板膜的完整性，以及 Caco-2 细胞中的 COX-1 和 COX-2 蛋白表达水平。这些结果表明，PDFOA 和 HDFNA 有可能通过抑制 COX 途径在活性水平上而不是在蛋白水平上调节血小板功能。
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