Elliott G R, Adolfs M J, Bonta I L
Eur J Pharmacol. 1985 Apr 16;110(3):367-71. doi: 10.1016/0014-2999(85)90566-7.
Arachidonic acid (AA) injected locally into carrageenin/sponge granulomas, but not if given orally, inhibited granuloma growth. Granuloma macrophage (M0) infiltration was inhibited, and prostaglandin E2 (PGE2) synthesis (ng/100 mg granuloma dry weight) stimulated, by AA treatment. M0 adenosine 3',5'-cyclic monophosphate (cAMP) levels and granuloma exudate volume were not affected. Granuloma M0s incubated in vitro with arachidonic acid synthesised thromboxane B2 (Txb2), 6-ketoprostaglandin F1 alpha (6-ketoPGF1 alpha), and preferentially, PGE2. The AA inhibition of granuloma growth was possibly mediated via the synthesis of PGE2.
将花生四烯酸(AA)局部注射到角叉菜胶/海绵肉芽肿中可抑制肉芽肿生长,但口服则无此效果。AA处理可抑制肉芽肿巨噬细胞(M0)浸润,并刺激前列腺素E2(PGE2)合成(ng/100mg肉芽肿干重)。M0的3',5'-环磷酸腺苷(cAMP)水平和肉芽肿渗出液体积不受影响。体外与花生四烯酸孵育的肉芽肿M0合成了血栓素B2(Txb2)、6-酮前列腺素F1α(6-酮PGF1α),且优先合成了PGE2。AA对肉芽肿生长的抑制可能是通过PGE2的合成介导的。