Gotteland M, Cruchet S, Verbeke S
Gastroenterology Unit, Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile.
Aliment Pharmacol Ther. 2001 Jan;15(1):11-7. doi: 10.1046/j.1365-2036.2001.00898.x.
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.
To determine whether ingestion of the probiotic Lactobacillus GG (LGG) protects the gastrointestinal mucosa against indometacin-induced alterations of permeability.
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.
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.
Regular ingestion of LGG protects the integrity of the gastric mucosal barrier against indometacin, but has no effect at the intestinal level.
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。
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。
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。
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。