Cirino G, Cicala C, Sorrentino L, Ciliberto G, Arpaia G, Perretti M, Flower R J
Department of Experimental Pharmacology, University of Naples-Federico II, Italy.
Br J Pharmacol. 1993 Mar;108(3):573-4. doi: 10.1111/j.1476-5381.1993.tb12843.x.
An acetylated polypeptide corresponding to residues 2-26 of human lipocortin 1 was synthesized and the anti-inflammatory activity assessed in three models of acute inflammation in rat and mouse. In the carrageenin rat paw oedema test, the peptide produced a maximal inhibition of approximately 41% at the 3 h time point with a 10 micrograms dose. When rat paw oedema was induced by the injection of venom phospholipase A2, the peptide produced a significant inhibition (31%) at the top dose of 20 micrograms per paw. In the mouse air-pouch model, systemic treatment with the peptide produced a dramatic reduction in cytokine-induced leukocyte migration with an ID50 of approximately 40 micrograms per mouse. The N-terminal peptide 2-26 shares the actions of lipocortin 1 in these acute models of inflammation.
合成了一种与人脂皮质素1第2至26位残基相对应的乙酰化多肽,并在大鼠和小鼠的三种急性炎症模型中评估了其抗炎活性。在角叉菜胶诱导的大鼠足爪水肿试验中,10微克剂量的该多肽在3小时时间点产生了约41%的最大抑制率。当通过注射毒液磷脂酶A2诱导大鼠足爪水肿时,该多肽在每只足爪20微克的最高剂量下产生了显著抑制(31%)。在小鼠气囊模型中,该多肽全身给药使细胞因子诱导的白细胞迁移显著减少,半数抑制剂量约为每只小鼠40微克。N端多肽2 - 26在这些急性炎症模型中具有与人脂皮质素1相同的作用。