植物油乳治疗胃溃疡的实验与临床研究

目的：对两种植物油乳──鸦胆子油乳（简称鸦乳）和豆油乳治疗胃溃疡的作用进行观察。方法：首先观察鸦乳对四种胃溃疡动物模型的疗效，进而探讨其对动物胃粘膜内源性PGE2、MDA、SOD活性和氧自由基相对含量的影响，然后通过开放性临床观察和随机双盲对照试验观察其临床疗效。结果：鸦乳对四种胃溃疡动物模型均有疗效（P＜0．01）；豆油乳对应激性胃溃疡动物模型亦有疗效，作用与鸦乳比较，差异无显著性（P＞0．05）；鸦乳增加动物及人体胃粘膜内源性PGE2（P＜0．01），降低动物胃粘膜SOD活性（P＜0．01），减低动物胃粘膜MDA和氧自由基相对含量（P＜0．01）。开放性临床观察及随机双盲对照临床观察均显示，鸦乳治疗胃溃疡的8周有效率＞91．62％，8周愈合率＞75％，疗效优于对照剂西咪替丁（国产）和石蜡油乳（P＜0.01），未发现不良反应。结论：鸦乳和豆油乳治疗胃溃疡的疗效是肯定的，其主要作用机理是增加胃粘膜内源性PGE2、减轻氧自由基对胃粘膜的损害。

Experimental study and clinical trials of emulsion of plant oil in treatment of gastric ulcer

Objective: The therapeutic effect of emulsion of semenal oil of brucea javanica (ESOBJ) and emulsion of soybean oil, Intralipid on gastric ulcer were observed. Methods: The therapeutic effects of ESOBJ and its components, seminal oil of brueea javanica (SOBJ) and phospholipid were observed on stress ulcer, aspirin, pylorus-ligated and acetic acid ulcer models in mice and rats. Concomitently, therapeutic effect of emulsion of soybean oil on mice stress ulcer was observed, all with distilled water used as placebo. An open trial and a double-blind randomized controlled clinical trial were carried out in two stages, on outpatients. Results: SOBJ has better effect on gastric ulcer models than the placebo (P<0.01). Whereas phospholipid alon was not (P>0.05). Pepsin activity (P<0.01), SOD(P<0.01) and MDA(P<0.01) in animals, gastric mucosa were reduced while endogenous PGE2 in animals and patients' gastric mucosa were increased. Emulsion of soybean oil was significantly superior over the placebo on stress ulcer model therapeutically, but with no difference in efficacy as compared with ESOBJ. Unsaturated fatty acids were detected in ESOBJ and soybean oil, these substances seem to be related to the protective mechanism of gastric mucosa. The above results indicated that ESOBJ was significantly superior to cimetidine (domestic product) (P<0.01) and emulsion of mineral oil (P<0.01). Conclusions: Emulsion of plant oil, ESOBJ and emulsion of soybean oil are effective in treatment of gastric ulcer. Their mechanism of actions may involve: increase of endogenous PGE2 in gastric mucosa; reduced damage induced by free radical.