兔皮肤对局部应用花生四烯酸的炎症反应及其药理调节。
The inflammatory response of rabbit skin to topical arachidonic acid and its pharmacological modulation.
作者信息
Aked D, Foster S J, Howarth A, McCormick M E, Potts H C
出版信息
Br J Pharmacol. 1986 Oct;89(2):431-8. doi: 10.1111/j.1476-5381.1986.tb10277.x.
The inflammatory reaction induced by the intradermal injection of arachidonic acid into the rabbit dermis has been investigated. Plasma extravasation was measured by the leakage of 125I-albumin into the tissues and polymorphonuclear leukocyte (PMNL) accumulation was assessed histologically. Arachidonic, 5,8,11,14,17-eicosapentaenoic and 8,11,14-eicosatrienoic acids, but not oleic, linoleic or linolenic acids, caused a concentration-related plasma extravasation following their intra-dermal injection. The plasma extravasation induced by arachidonic acid was dependent on PMNLs. PMNL infiltration and plasma extravasation into arachidonic acid-injected skin sites was inhibited by the mixed cyclo-oxygenase-lipoxygenase inhibitor, BW755C. Arachidonic acid-induced plasma extravasation was inhibited by cyclo-oxygenase and 5-lipoxygenase inhibitors but not by the Paf antagonist, kadsurenone. The inflammation induced by arachidonic acid in the rabbit dermis may be a useful model for evaluating 5-lipoxygenase inhibitors which could be potentially useful anti-inflammatory agents for the treatment of psoriasis and other inflammatory diseases.
已对向兔真皮内注射花生四烯酸所诱导的炎症反应进行了研究。通过125I-白蛋白向组织中的渗漏来测定血浆渗出，并通过组织学方法评估多形核白细胞（PMNL）的积聚。花生四烯酸、5,8,11,14,17-二十碳五烯酸和8,11,14-二十碳三烯酸，但油酸、亚油酸或亚麻酸不会，在皮内注射后会引起浓度相关的血浆渗出。花生四烯酸诱导的血浆渗出依赖于PMNL。混合的环氧化酶-脂氧合酶抑制剂BW755C可抑制PMNL浸润和血浆向注射花生四烯酸的皮肤部位的渗出。花生四烯酸诱导的血浆渗出受到环氧化酶和5-脂氧合酶抑制剂的抑制，但不受血小板活化因子拮抗剂海风藤酮的抑制。花生四烯酸在兔真皮中诱导的炎症可能是一种用于评估5-脂氧合酶抑制剂的有用模型，这些抑制剂可能是治疗银屑病和其他炎症性疾病的潜在有用抗炎剂。
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