THE MECHANISM OF CARRAGEENAN INDUCED INFLAMMATION IN RAT

在用与浓度相关的 角叉菜胶（100 μ g/m1），先前标记的分离的胸膜巨噬细胞 （14 C）花生四烯酸释放的放射性是对照的2.5倍 细胞 释放的放射性物质的主要成分是 花生四烯酸和，在更小程度上，PGE 2和白三烯C4， 已知这两种物质都具有血管活性。 在没有角叉菜胶的情况下， 吲哚美辛（20 μ m）增加花生四烯酸的释放， 抑制PGE 2的形成，这意味着 静息的胸膜巨噬细胞能够将释放的 花生四烯酸转化为PGE 2。 角叉菜胶可以刺激 来自胸膜巨噬细胞的花生四烯酸表明， 磷脂酶A2参与卡拉胶的作用，PGE 2和 LTC 4可能介导角叉菜胶的体内炎症反应。 此外，我们的研究结果表明，巨噬细胞可能发挥作用， 炎症反应早期事件的开始。

Upon incubation with pharmacologically relevant concentrations of carrageenan (100 Mug/m1), isolated pleural macrophages previously labeled with (14C)arachidonic acid released 2.5 times the radioactivity of control cells. The main components of the released radioactive materials were arachidonic acid and, to a much lesser extent, PGE2 and leukotriene C4, both of which are known to be vasoactive. In the absence of carrageenan, indomethacin (20 Mum) augmented the release of arachidonic acid but suppressed the formation of PGE2, implying that the cyclooxygenase in resting pleural macrophages is capable of converting the released arachidonic acid to PGE2. That carrageenan can stimulate release of arachidonic acid from pleural macrophages indicates that activation of phospholipase A2 is involved in the carcageenan action and that PGE2 and LTC4 may mediate the inflammatory response to carrageenan in vivo. Furthermore, our findings suggest that the macrophages may play a role in the initiation of the early event in the inflammatory response.