Heiman A S, Crews F T
Prostaglandins. 1984 Feb;27(2):335-43. doi: 10.1016/0090-6980(84)90084-4.
Purified rat mst cells were used to study the effects of antiinflammatory steroids on the release of [1-14C]-arachidonic acid ([1-14C]AA) and metabolites. Mast cell were incubated overnight with glucocorticoids, [1-14C]AA incorporated into cellular phospholipids and the release of [1-14C]AA, and metabolites determined using a variety of secretagogues. Release of [1-14C]AA and metabolites by concanavalin A, the antigen ovalbumin and anti-immunoglobulin E antibody was markedly reduced by glucocorticoid treatment. Neither the total incorporation of [1-14C]AA nor the distribution into phospholipids was altered by hydrocortisone pretreatment. Glucocorticoid pretreatment did not alter [1-14C]AA release stimulated by somatostatin, compound 48/80, or the calcium ionophore, A23187. These data indicate that antiinflammatory steroids selectively inhibit immunoglobulin dependent release of arachidonic acid from rat mast cells. These findings question the role of lipomodulin and macrocortin as general phospholipase inhibitors and suggest that they may be restricted to immunoglobulin stimuli.
纯化的大鼠肥大细胞被用于研究抗炎类固醇对[1-14C] -花生四烯酸([1-14C] AA)及其代谢产物释放的影响。肥大细胞与糖皮质激素一起孵育过夜,[1-14C] AA掺入细胞磷脂中,然后使用多种促分泌剂测定[1-14C] AA及其代谢产物的释放。糖皮质激素处理显著降低了伴刀豆球蛋白A、抗原卵清蛋白和抗免疫球蛋白E抗体引起的[1-14C] AA及其代谢产物的释放。氢化可的松预处理既未改变[1-14C] AA的总掺入量,也未改变其在磷脂中的分布。糖皮质激素预处理未改变生长抑素、化合物48/80或钙离子载体A23187刺激的[1-14C] AA释放。这些数据表明抗炎类固醇选择性抑制大鼠肥大细胞中免疫球蛋白依赖性花生四烯酸的释放。这些发现质疑了脂调素和巨皮质素作为一般磷脂酶抑制剂的作用,并表明它们可能仅限于免疫球蛋白刺激。