THE MECHANISM OF CARRAGEENAN INDUCED INFLAMMATION IN RAT

从大鼠胸腔中分离出的细胞主要由 巨噬细胞、肥大细胞、嗜酸性粒细胞、淋巴细胞和间皮细胞。 释放标记[14C]-花生四烯酸的分离胸膜细胞 在药物作用下暴露于大量的放射性标记 相应浓度的角叉菜胶(L-100ug/ml)。的时间进程 释放也与体内炎症作用相一致。 卡拉胶。磷脂酶A2的抑制剂(即对溴苯乙酰 溴)，但不是花生四烯酸环氧合酶(即消炎痛) 抑制药物释放，呈剂量依赖关系。分析(高效液相色谱仪和 放射免疫分析)的发布产品表明，90%以上 放射性标记为花生四烯酸。卡拉胶还引起了显著的 胸膜细胞释放乳酸脱氢酶(LDH)。乳酸脱氢酶的释放 一般平行释放放射性标签，尽管释放放射性标签 早于乳酸脱氢酶。这两件事没有因果关系 然而，这种关系通过对溴苯酰基的失败而得到证明 溴化物以阻止乳酸脱氢酶的释放。

Cells isolated from the pleural cavity of rat consisted mainly of macrophages, mast cells, eosinophils, lymphocytes and mesothelial cells. Isolated pleural cells labeled with [14C]-arachidonic acid released substantial amounts of radiolabel upon exposure to pharmacologically relevant concentration of carrangeenan (l-100 ug/ml). The time course of release was also compatible with the in vivo inflammatory action of carrageenan. An inhibitor of phospholipase A2 (i.e., p-bromophenacyl bromide) but not of arachidonate cyclooxygenase (i.e., indomethacin) inhibited the release in a dose-dependent manner. Analysis (by HPLC and radioimmunoassay) of the released products indicated that more than 90% of the radiolabel was arachidonic acid. Carrageenan also caused significant release of lactate dehydrogenase (LDH) from pleural cells. Release of LDH generally paralleled release of radiolabel although release of radiolabel preceded that of LDH. That the two events did not bear a cause-effect relationship, however, was demonstrated by the failure of p-bromophenacyl bromide to block release of LDH.