Arachidonic acid stimulates corneal epithelial migration.

M Nakamura, T Fujihara, H Mibu, M Hikida
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引用次数: 11

Abstract

We determined the concentration dependent effects of arachidonic acid between 0.3 and 30 x 10(-6) M on corneal epithelial migration, in an organ culture system of the rabbit cornea. With 3 x 10(-6) M arachidonic acid, corneal epithelial migration was maximally stimulated by 51%. The cyclooxygenase inhibitors, indomethacin, ketoprofen, flurbiprofen and diclofenac sodium also all had a tendency to stimulate corneal epithelial migration at low concentrations (0.1 or 1 x 10(-6) M). However, the inhibitory effect of epithelial migration was observed at higher concentration (100 x 10(-6) M) of these compounds. On the other hand, the selective 5-lipoxygenase inhibitor, AA-861 over a concentration range from 0.1 to 10 x 10(-6) M maximally inhibited corneal epithelial migration by 25%. These results suggest that during wound healing some of the increased release of arachidonic acid may be derived from a metabolite of the 5-lipoxygenase pathway which may in turn hasten wound closure.

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花生四烯酸刺激角膜上皮细胞迁移。
我们测定了花生四烯酸在0.3和30 × 10(-6) M之间对兔角膜器官培养系统中角膜上皮迁移的浓度依赖性效应。3 × 10(-6) M花生四烯酸对角膜上皮迁移的刺激最大,达到51%。环氧合酶抑制剂、吲哚美辛、酮洛芬、氟比洛芬和双氯芬酸钠在低浓度(0.1或1 × 10(-6) M)时也都有刺激角膜上皮迁移的倾向,但在较高浓度(100 × 10(-6) M)时,这些化合物对上皮迁移的抑制作用被观察到。另一方面,选择性5-脂氧合酶抑制剂AA-861在0.1至10 × 10(-6) M的浓度范围内最大限度地抑制了25%的角膜上皮迁移。这些结果表明,在伤口愈合过程中,花生四烯酸的一些增加释放可能来自5-脂氧合酶途径的代谢物,这可能反过来加速伤口愈合。
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