Protection of the gastric mucosa by linoleic acid--a nutrient essential fatty acid.

We studied whether linoleic acid, a precursor for arachidonic acid and prostaglandins, could protect the gastric mucosa against ethanol-induced injury. Fasted male rats received intragastric pretreatment with 1 ml of one of: a) solubilizer; b) solubilized linoleic acid (74 mg); or c) solubilized oleic acid (74 mg) (a nonessential fatty acid). One hour later, 2 ml 100% ethanol was given intragastrically. Three hours after ethanol administration, the gastric mucosa was assessed for gross necrosis and for histologic changes. Three hours after ethanol administration in solubilizer, pretreated-group gross mucosal necrosis involved 35 +/- 3% of total mucosal area, while deep histologic necrosis involved 52 +/- 4% of the mucosal strip length. Pretreatment with linoleic acid (but not oleic acid) significantly reduced gross histologic necrosis, to 2.3 +/- 0.5%, and deep histologic necrosis to 4 +/- 2% (both p less than 0.001 versus solubilizer group). The protective action of linoleic acid was significantly reduced (greater than 10-fold) by pretreatment with indomethacin (prostaglandins synthetase inhibitor), suggesting prostaglandins as mediators of protection. The present study showed that effective protection of the gastric mucosa against ethanol injury can be achieved by intragastric administration of linoleic acid, a dietary essential fatty acid.

我们研究了亚油酸（花生四烯酸和前列腺素的前体）是否能够保护胃黏膜免受乙醇诱导的损伤。禁食的雄性大鼠接受胃内预处理，分别给予1毫升以下物质之一：a) 增溶剂；b) 增溶的亚油酸（74毫克）；c) 增溶的油酸（74毫克）（一种非必需脂肪酸）。1小时后，胃内给予2毫升100%乙醇。乙醇给药3小时后，对胃黏膜进行大体坏死评估和组织学变化评估。在给予增溶剂并乙醇给药3小时后，预处理组的胃黏膜大体坏死占黏膜总面积的35 ± 3%，而深层组织学坏死占黏膜条长度的52 ± 4%。亚油酸预处理（而非油酸）显著减少了大体组织学坏死，降至2.3 ± 0.5%，深层组织学坏死降至4 ± 2%（与增溶剂组相比，两者均P < 0.001）。用吲哚美辛（前列腺素合成酶抑制剂）预处理后，亚油酸的保护作用显著降低（大于10倍），这表明前列腺素是保护作用的介质。本研究表明，通过胃内给予亚油酸（一种膳食必需脂肪酸），可以有效保护胃黏膜免受乙醇损伤。