Arachidonic acid-derived prostaglandins are widely studied for their role in inflammation. However, besides arachidonic acid, other arachidonic moiety-containing lipids can be metabolized by COX-2. Indeed, the endocannabinoids 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamine (anandamide, AEA) can follow the same biochemical pathways than arachidonic acid leading to the formation of prostaglandin-glycerol esters (PG-G) and prostaglandin-ethanolamides (or prostamides, PG-EA), respectively.

The data reported so far support the interest of these bioactive lipids in inflammatory conditions. However, there is only a handful of methods described for their quantification in biological matrices. Moreover, given the shared biochemical pathways for arachidonic acid, 2-AG and AEA, a method allowing for the quantification of these precursors and the corresponding prostaglandin derivatives appears as largely needed. Thus, we report here the development and validation of a single run UPLC-MS/MS quantification method allowing the quantification of these endocannabinoids-derived mediators together with the classical prostaglandin. Moreover, we applied the method to the quantification of these lipids in vitro (using lipopolysaccharides-activated J774 macrophage cells) and in vivo in several tissues from DSS-induced colitis mice. This femtomole-range method should improve the understanding of the interaction between these lipid mediators and inflammation.

花生四烯酸衍生的前列腺素因其在炎症中的作用而被广泛研究。然而，除了花生四烯酸之外，其他含有花生四烯酸部分的脂质也可以被COX-2代谢。事实上，内源性大麻素 2-花生四烯酰甘油 (2-AG) 和N-花生四烯酰乙醇胺（anandamide，AEA）可以遵循与花生四烯酸相同的生化途径，导致前列腺素甘油酯 (PG-G) 和前列腺素乙醇酰胺（或前列腺酰胺，PG-EA）。

迄今为止报道的数据支持这些生物活性脂质在炎症条件下的作用。然而，仅描述了少数几种在生物基质中进行定量的方法。此外，鉴于花生四烯酸、2-AG 和 AEA 具有共同的生化途径，因此迫切需要一种能够定量这些前体和相应前列腺素衍生物的方法。因此，我们在此报告单次运行 UPLC-MS/MS 定量方法的开发和验证，该方法允许对这些内源性大麻素衍生的介质与经典前列腺素一起进行定量。此外，我们将该方法应用于体外（使用脂多糖激活的 J774 巨噬细胞）和 DSS 诱导的结肠炎小鼠的几种组织中的体内这些脂质的定量。这种飞摩尔范围的方法应该可以提高对这些脂质介质与炎症之间相互作用的理解。