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摄入乳酸杆菌对消炎痛诱导的人体胃肠道黏膜屏障改变的影响。

Effect of Lactobacillus ingestion on the gastrointestinal mucosal barrier alterations induced by indometacin in humans.

作者信息

Gotteland M, Cruchet S, Verbeke S

机构信息

Gastroenterology Unit, Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile.

出版信息

Aliment Pharmacol Ther. 2001 Jan;15(1):11-7. doi: 10.1046/j.1365-2036.2001.00898.x.

Abstract

BACKGROUND

Chronic nonsteroidal anti-inflammatory drug (NSAID) ingestion strongly affects the gastrointestinal mucosa as a first stage before ulceration. Some Lactobacillus strains may stabilize the mucosal barrier by increasing mucin expression, reducing bacterial overgrowth, stimulating mucosal immunity and synthetizing antioxidant substances; these events are altered in NSAID-associated gastroenteropathy.

AIM

To determine whether ingestion of the probiotic Lactobacillus GG (LGG) protects the gastrointestinal mucosa against indometacin-induced alterations of permeability.

SUBJECTS AND METHODS

Four gastrointestinal permeability tests were carried out in random order in 16 healthy volunteers: (i) basal; (ii) after indometacin; (iii) after 5 days of living LGG ingestion before indometacin administration; (iv) after 5 days of heat-killed LGG ingestion before indometacin administration.

RESULTS

Indometacin significantly increased basal sucrose urinary excretion (29.6 mg [17.1-42.1] vs. 108.5 mg [68.2-148.7], P=0.0030) (means [95% CI]) and lactulose/mannitol urinary excretion (1.03% [0.73-1. 32] vs. 2.93% [1.96-3.90], P=0.00012). Heat-killed LGG did not modify the indometacin-induced increase of gastrointestinal permeability, while live bacteria significantly reduced the alteration of gastric (47.8 mg [31.1-64.6], P=0.012) but not intestinal permeability induced by NSAID.

CONCLUSIONS

Regular ingestion of LGG protects the integrity of the gastric mucosal barrier against indometacin, but has no effect at the intestinal level.

摘要

背景

长期服用非甾体抗炎药(NSAID)在溃疡形成前的第一阶段会对胃肠道黏膜产生强烈影响。一些乳酸杆菌菌株可通过增加黏蛋白表达、减少细菌过度生长、刺激黏膜免疫和合成抗氧化物质来稳定黏膜屏障;这些过程在NSAID相关性胃肠病中会发生改变。

目的

确定摄入益生菌鼠李糖乳杆菌GG(LGG)是否能保护胃肠道黏膜免受吲哚美辛引起的通透性改变。

对象与方法

对16名健康志愿者随机进行四项胃肠道通透性测试:(i)基础测试;(ii)服用吲哚美辛后;(iii)在服用吲哚美辛前连续5天摄入活的LGG后;(iv)在服用吲哚美辛前连续5天摄入热灭活的LGG后。

结果

吲哚美辛显著增加了基础尿蔗糖排泄量(29.6 mg [17.1 - 42.1] 对比108.5 mg [68.2 - 148.]],P = 0.0030)(均值 [95% 置信区间])以及乳果糖/甘露醇尿排泄量(1.03% [0.73 - 1.32] 对比2.93% [1.96 - 3.90],P = 0.00012)。热灭活的LGG并未改变吲哚美辛引起的胃肠道通透性增加,而活菌显著降低了NSAID引起的胃通透性改变(47.8 mg [31.1 - 64.6],P = 0.012),但对肠道通透性无影响。

结论

定期摄入LGG可保护胃黏膜屏障免受吲哚美辛的破坏,但对肠道水平无作用。

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