Duval D
Presse Med. 1986 Mar 1;15(9):433-5.
In most of the cell types hitherto investigated in vitro, glucocorticoids have been shown to decrease the synthesis of prostaglandins and of lipoxygenase derivatives of arachidonic acid. This effect seems to be related to the induction of protein inhibitors of phospholipase A2. Several of these inhibitors, called lipocortins, have recently been identified in leucocytes, macrophages and rat renomedullary cell cultures. However, systemic treatment with glucocorticoids in animals and in man has generally failed to induce a significant decrease in either urinary excretion or plasma concentration of prostaglandins. These results suggest that inhibition of prostaglandin synthesis is not the only mechanism explaining the anti-inflammatory action of glucocorticoids and raise the question of the physiological role of lipocortins.
在迄今为止体外研究的大多数细胞类型中，糖皮质激素已被证明可减少前列腺素以及花生四烯酸脂氧合酶衍生物的合成。这种作用似乎与磷脂酶A2蛋白抑制剂的诱导有关。最近在白细胞、巨噬细胞和大鼠肾髓质细胞培养物中鉴定出了几种这类抑制剂，称为脂皮质素。然而，在动物和人类中全身应用糖皮质激素通常未能使前列腺素的尿排泄或血浆浓度显著降低。这些结果表明，抑制前列腺素合成并非解释糖皮质激素抗炎作用的唯一机制，并引发了脂皮质素生理作用的问题。
