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Role of melatonin in mucosal gastroprotection against aspirin-induced gastric lesions in humans.
Journal of Pineal Research ( IF 10.3 ) Pub Date : 2010-05-06 , DOI: 10.1111/j.1600-079x.2010.00755.x
P C Konturek 1 , S J Konturek , K Celinski , M Slomka , H Cichoz-Lach , W Bielanski , R J Reiter
Affiliation  

Melatonin and its precursor, l-tryptophan, have been shown to exert gastroprotective effects in animals, but their influence on the gastric damage by aspirin (ASA) in humans has been sparingly investigated. In this study, we designed to determine the effects of melatonin and l-tryptophan on ASA-induced gastric mucosal damage, gastric microbleeding, mucosal generation of prostaglandin E(2), and plasma melatonin, and gastrin levels. Three groups of healthy male volunteers (n = 30) with intact gastric mucosa received daily for 11 days either ASA alone or that combined with melatonin or tryptophan. Gastric blood loss and mucosal damage were evaluated at 3rd, 7th, and 11th days of ASA administration by endoscopy using Lanza score. ASA alone caused a marked rise of gastric damage and gastric blood loss, mainly at day 3rd and 7th, but they were significantly reduced at 11th day. Pretreatment with melatonin or tryptophan remarkably reduced ASA induced gastric lesions and microbleeding. Gastric mucosal generation of PGE(2) was suppressed by about 90% in all subjects treated with ASA alone without or with addition of melatonin or tryptophan. Plasma melatonin was markedly increased after treatment with melatonin or tryptophan plus ASA, but it was also raised significantly after application of ASA alone. Plasma gastrin levels were raised in subjects given melatonin or tryptophan plus ASA, but not in those with ASA alone. We conclude that melatonin and its precursor tryptophan given orally significantly reduce gastric lesions induced by ASA possibly due to (a) direct gastroprotective action of exogenous melatonin or that generated from tryptophan and (b) gastrin released from the gastric mucosa by melatonin or tryptophan.

中文翻译:

褪黑素在针对人类阿司匹林诱发的胃部损伤的粘膜胃保护中的作用。

褪黑素及其前体1-色氨酸已显示出对动物具有胃保护作用,但对阿司匹林(ASA)对人的胃部损害的影响却很少进行研究。在这项研究中,我们设计确定褪黑素和l-色氨酸对ASA诱导的胃粘膜损害,胃微出血,前列腺素E(2)的粘膜生成,血浆褪黑激素和胃泌素水平的影响。三组健康的胃粘膜完整男性志愿者(n = 30)每天接受ASA单独治疗或与褪黑素或色氨酸联合治疗11天。使用Lanza评分通过内窥镜检查在ASA给药的第3天,第7天和第11天评估胃失血和粘膜损伤。仅在第3天和第7天,仅ASA会引起明显的胃损伤和胃失血,但在第11天时它们显着减少。褪黑素或色氨酸预处理可显着减少ASA诱发的胃部病变和微出血。在不使用或不添加褪黑素或色氨酸的单独用ASA治疗的所有受试者中,PGE(2)的胃粘膜生成被抑制了约90%。褪黑素或色氨酸加ASA处理后,血浆褪黑素显着增加,但单独使用ASA后,血浆褪黑素也显着增加。服用褪黑素或色氨酸加ASA的受试者血浆中胃泌素水平升高,但仅使用ASA的受试者血浆中胃泌素水平升高。
更新日期:2010-04-08
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