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花生四烯酸对大鼠黏膜应激性溃疡的保护作用。

Arachidonic acid protection of rat mucosa against stress ulceration.

作者信息

Auguste L J, Angus L, Stein T A, Wise L

出版信息

J Surg Res. 1987 Jul;43(1):103-6. doi: 10.1016/0022-4804(87)90053-9.

Abstract

To evaluate the effect of arachidonic acid (AA), a prostaglandin precursor, on the mucosal level of PGE2 and its possible protective role against stress ulcerations, 40 Holtzman rats were divided into four groups: Group I intragastrically receiving 1 ml of normal saline (NS); Group II, NS pretreatment followed by stress; Group III, intragastric AA pretreatment without stress; and Group IV, intragastric AA followed by stress. AA was administered as a 120 mM solution in a nonionic detergent, adjusted to a pH of 8.0. Stress was provided by the cold-restraint method. After sacrifice, the number of gastric mucosal ulcerations were counted. Specimens of nonulcerated mucosa were assayed for PGE2 by derivatization with panacyl bromide and by using high-performance liquid chromatography. The animals in Groups I, III, and IV developed no gastric ulcerations and their mucosal prostaglandin E2 remained at a normal level, while those in Group II had a significant reduction of mucosal PGE2 (P less than 0.05) and a significantly increased number of gastric ulcerations (P less than 0.002). These data indicate that stress-induced mucosal ulcerations are associated with significant decreases in the gastric mucosal levels of PGE2. Intragastric administration of arachidonic acid prevents the formation of stress mucosal ulcerations and maintains a normal level of mucosal PGE2.

摘要

为评估前列腺素前体花生四烯酸(AA)对胃黏膜PGE2水平的影响及其对应激性溃疡的可能保护作用,将40只霍尔茨曼大鼠分为四组:第一组经胃内给予1 ml生理盐水(NS);第二组,NS预处理后施加应激;第三组,胃内给予AA预处理但无应激;第四组,胃内给予AA后施加应激。AA以120 mM溶液的形式溶于非离子去污剂中,调节pH值至8.0。通过冷束缚法施加应激。处死后,计算胃黏膜溃疡的数量。用泛酰溴衍生化并采用高效液相色谱法对未溃疡黏膜标本进行PGE2检测。第一组、第三组和第四组动物未出现胃溃疡,其黏膜前列腺素E2水平保持正常,而第二组动物的黏膜PGE2显著降低(P<0.05),胃溃疡数量显著增加(P<0.002)。这些数据表明,应激诱导的黏膜溃疡与胃黏膜PGE2水平显著降低有关。胃内给予花生四烯酸可预防应激性黏膜溃疡的形成,并维持黏膜PGE2的正常水平。

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