Jiménez P, Lanas A, Piazuelo E, Bioque G, Esteva F
Unidad Mixta de Investigación, University of Zaragoza, Spain.
Inflammation. 1997 Aug;21(4):419-29. doi: 10.1023/a:1027318520752.
Unlike gastric mucosa, it has been considered that lipoxygenase metabolites protect the esophageal mucosa and that prostaglandins are only secreted in the presence of esophageal inflammation. The aim of this study was to determine the profile of arachidonic acid metabolites and their response to regulatory compounds in rabbit esophageal mucosal cells in culture. Eicosanoids secreted into the medium were extracted and identified by HPLC and RIA. Esophageal mucosal cells in culture metabolized arachidonic acid mainly through the cycloxygenase pathway and PGE2 was the major arachidonic acid metabolite secreted. The addition of IL-1 beta and A23187 (calcium ionophore) stimulated PGE2 synthesis. In basal conditions neither leukotrienes nor HETEs were detected. However, the addition of the NDGA induced the secretion of lipoxygenase metabolites identified as 12-15 HETEs. In conclusion, rabbit esophageal epithelial cells in culture metabolize arachidonic acid via both cycloxygenase and lipoxygenase pathways. In our system, PGE2 was the main arachidonic acid metabolite.
与胃黏膜不同，人们一直认为脂氧合酶代谢产物可保护食管黏膜，且前列腺素仅在食管发生炎症时才会分泌。本研究的目的是确定培养的兔食管黏膜细胞中花生四烯酸代谢产物的概况及其对调节化合物的反应。通过高效液相色谱法（HPLC）和放射免疫分析法（RIA）提取并鉴定分泌到培养基中的类花生酸。培养的食管黏膜细胞主要通过环氧化酶途径代谢花生四烯酸，且前列腺素E2（PGE2）是分泌的主要花生四烯酸代谢产物。添加白细胞介素-1β（IL-1β）和A23187（钙离子载体）可刺激PGE2的合成。在基础条件下，未检测到白三烯和羟二十碳四烯酸（HETEs）。然而，添加去甲二氢愈创木酸（NDGA）可诱导分泌被鉴定为12-15 HETEs的脂氧合酶代谢产物。总之，培养的兔食管上皮细胞通过环氧化酶和脂氧合酶途径代谢花生四烯酸。在我们的系统中，PGE2是主要的花生四烯酸代谢产物。
