Cirino G, Peers S H, Flower R J, Browning J L, Pepinsky R B
Pharmacology Group, School of Pharmacy and Pharmacology, University of Bath, Claverton Down, United Kingdom.
Proc Natl Acad Sci U S A. 1989 May;86(9):3428-32. doi: 10.1073/pnas.86.9.3428.
Human recombinant lipocortin 1 has been tested for anti-inflammatory activity in a conventional model of acute inflammation. Microgram amounts of the protein, locally administered, inhibited edema of the rat paw when induced by subplantar injections of carrageenin: the ED50 was 10-20 micrograms per paw, and inhibition (maximum of 60-70%) was not dependent upon an intact adrenal cortex. Doses of lipocortin that produced approximately 50% inhibition in the carrageenin test were inactive against edema elicited by bradykinin, serotonin, platelet-activating factor-acether, or dextran, whereas edema caused by Naja mocambique venom phospholipase A2 was strongly inhibited by lipocortin. The protein inhibited edema when rats were pretreated with agents that depleted mast-cell amines, kininogen, or polymorphonuclear leukocytes prior to initiation of the carrageenin edema but had no inhibitory action when rats were pretreated with the dual cyclooxygenase/lipoxygenase inhibitor BW 755C. These results demonstrate that human recombinant lipocortin has potent local anti-inflammatory activity, probably through selectively interfering with eicosanoid generation. Lipocortin is relatively ineffective against edema caused by mast-cell degranulation or kinins, except when degranulation is caused by phospholipase A2.
已在急性炎症的传统模型中对人重组脂皮质蛋白1的抗炎活性进行了测试。局部给予微克量的该蛋白,可抑制由角叉菜胶足底注射诱导的大鼠爪水肿:半数有效量为每只爪10 - 20微克,且抑制作用(最大可达60 - 70%)不依赖于完整的肾上腺皮质。在角叉菜胶试验中产生约50%抑制作用的脂皮质蛋白剂量,对缓激肽、5 - 羟色胺、血小板活化因子 - 乙醚或右旋糖酐引起的水肿无活性,而莫桑比克眼镜蛇毒磷脂酶A2引起的水肿则被脂皮质蛋白强烈抑制。当在角叉菜胶水肿开始前用耗尽肥大细胞胺、激肽原或多形核白细胞的药物预处理大鼠时,该蛋白可抑制水肿,但当用双环氧合酶/脂氧合酶抑制剂BW 755C预处理大鼠时则无抑制作用。这些结果表明,人重组脂皮质蛋白具有强大的局部抗炎活性,可能是通过选择性干扰类花生酸的生成。脂皮质蛋白对肥大细胞脱颗粒或激肽引起的水肿相对无效,除非脱颗粒是由磷脂酶A2引起的。