Cirino G, Sorrentino L
Agents Actions. 1986 Aug;18(5-6):535-7. doi: 10.1007/BF01964960.
The effects of drugs which interfere with arachidonate metabolism as well as glucocorticoid-induced anti-phospholipase proteins (APP) have been studied on PGI2 generation by rat stomach tissue. Indomethacin inhibited PGI2 generation both in vitro and ex vivo while dexamethasone was ineffective in both instances. APP inhibited PGI2 generation in vitro. The results are discussed in the light of the possible mode of action of glucocorticoids. Prostacyclin (PGI2) is the major cyclo oxygenase metabolite in the rat gastric mucosa and exerts gastroprotective actions. Therefore a correlation between the inhibition of PGI2 synthesis and the induction of gastric damage has been suggested for the non-steroidal anti-inflammatory drugs. Glucocorticoids inhibit phospholipase A2 (PLA2) by inducing in the target cells the synthesis of inhibitory proteins, the lipocortins, and consequently reduce the release of eicosanoids in a number of cells and tissues. However, there is a surprising paucity of information on the effect of glucocorticoids on arachidonic acid (AA) metabolism in the gastro-intestinal tract. Moreover, the relationship between steroid administration and gastric damage is still controversial. The present work was undertaken to investigate the effect of drugs which interfere with AA metabolism on the synthesis of PGI2 by rat stomach mucosa and by the underlying muscularis layer both in vitro and ex vivo.
已经研究了干扰花生四烯酸代谢的药物以及糖皮质激素诱导的抗磷脂酶蛋白（APP）对大鼠胃组织生成前列环素（PGI2）的影响。吲哚美辛在体外和体内均抑制PGI2的生成，而地塞米松在这两种情况下均无效。APP在体外抑制PGI2的生成。根据糖皮质激素可能的作用方式对结果进行了讨论。前列环素（PGI2）是大鼠胃黏膜中主要的环氧化酶代谢产物，并具有胃保护作用。因此，有人提出非甾体类抗炎药抑制PGI2合成与胃损伤诱导之间存在相关性。糖皮质激素通过在靶细胞中诱导抑制性蛋白脂皮质素的合成来抑制磷脂酶A2（PLA2），从而减少许多细胞和组织中类花生酸的释放。然而，关于糖皮质激素对胃肠道中花生四烯酸（AA）代谢的影响，目前令人惊讶地缺乏相关信息。此外，类固醇给药与胃损伤之间的关系仍存在争议。目前的工作旨在研究干扰AA代谢的药物对大鼠胃黏膜及其下层肌层在体外和体内生成PGI2的影响。
