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花生四烯酸代谢以及5,8,11,14-二十碳四炔酸和9a,12a-十八碳二炔酸对体外过敏反应的调节作用

Arachidonic acid metabolism and modulation of in vitro anaphylaxis by 5,8,11,14-eicosatetraynoic acid and 9a,12a-octadecadiynoic acid.

作者信息

Hitchcock M, Kokolis N A

出版信息

Br J Pharmacol. 1981 Apr;72(4):689-95. doi: 10.1111/j.1476-5381.1981.tb09150.x.

Abstract
  1. 5,8,11,14-Eicosatetraynoic acid (ETYA) inhibited the antigen-induced contractions of tracheal spirals obtained from actively sensitized guinea-pigs. Consistent data were obtained only when the spirals were treated with indomethacin. 2. ETYA did not affect histamine-induced contractions of indomethacin-treated tracheal spirals. 3. 9a, 12a-Octadecadiynoic acid (Ro-3-1314) a potential inhibitor of linoleic acid metabolism, stimulated the antigen-induced contraction of guinea-pig tracheal spirals and the immunological release of slow reacting substances of anaphylaxis (SRS-A) from actively sensitized guinea-pig lung fragments. 4. Both ETYA and Ro-3-1314 inhibited the immunological release of malondialdehyde from guinea-pig lung fragments. 5. The data indicate that the effects of ETYA were due to inhibition of lipoxygenase and the effects of Ro-3-1314 were due to inhibition of cyclo-oxygenase. 6. The results suggest that products of lipoxygenase contribute to the antigen-induced contraction of guinea-pig lung, particularly when cyclo-oxygenase is inhibited. Under these conditions there may be redirection of the metabolism of arachidonic acid to favour production of constrictor products of lipoxygenase such as SRS-A.
摘要
  1. 5,8,11,14-二十碳四炔酸(ETYA)抑制了从主动致敏豚鼠获得的气管螺旋条的抗原诱导收缩。仅当螺旋条用吲哚美辛处理时才获得一致的数据。2. ETYA不影响吲哚美辛处理的气管螺旋条的组胺诱导收缩。3. 9a,12a-十八碳二炔酸(Ro-3-1314),一种亚油酸代谢的潜在抑制剂,刺激了豚鼠气管螺旋条的抗原诱导收缩以及主动致敏豚鼠肺组织碎片中过敏反应慢反应物质(SRS-A)的免疫释放。4. ETYA和Ro-3-1314均抑制豚鼠肺组织碎片中丙二醛的免疫释放。5. 数据表明ETYA的作用是由于抑制脂氧合酶,而Ro-3-1314的作用是由于抑制环氧化酶。6. 结果表明脂氧合酶产物有助于豚鼠肺的抗原诱导收缩,特别是当环氧化酶被抑制时。在这些条件下,花生四烯酸的代谢可能会重新定向,以有利于产生脂氧合酶的收缩产物,如SRS-A。

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Arachidonate lipoxygenase in blood platelets.血小板中的花生四烯酸脂氧合酶。
Biochim Biophys Acta. 1975 Feb 20;380(2):299-307. doi: 10.1016/0005-2760(75)90016-8.

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