Lamine F, Fioramonti J, Bueno L, Nepveu F, Cauquil E, Lobysheva I, Eutamène H, Théodorou V
Neuro-Gastroenterology and Nutrition Unit, INRA, Toulouse, France.
Scand J Gastroenterol. 2004 Jan;39(1):37-45. doi: 10.1080/00365520310007152.
Beneficial effects of lactobacilli have been reported in experimental colitis. On the other hand, despite the controversial role of nitric oxide (NO) in the inflammatory gut process, a protective action of exogenous NO in inflammation has been suggested. Consequently, this study aimed to determine the effect of (i) sodium nitroprusside (SNP), a NO donor and (ii) treatment with Lactobacillus farciminis, which produces NO in vitro, on trinitrobenzene sulphonic acid (TNBS)-induced colitis in rats and to evaluate the role of exogenous NO in this effect.
Rats were divided into three groups receiving one of the following: (i) a continuous intracolonic (IC) infusion of SNP for 4 days, (ii) L. farciminis orally for 19 days, or (iii) saline. On day 1 and day 15, respectively, TNBS and saline were administrated IC, followed by a continuous IC infusion of saline or haemoglobin, a NO scavenger. At the end of treatments, the following parameters were evaluated: macroscopic damage of colonic mucosa, myeloperoxidase and nitric oxide synthase activities and colonic luminal NO production.
In colitic rats, SNP and L. farciminis treatment significantly (P < 0.05) reduced macroscopic damage scores, myeloperoxidase and nitric oxide synthase activities compared to controls. Haemoglobin infusion abolished the anti-inflammatory effect of both NO donor treatments, but had no effect per se on colitis.
NO released intraluminally by SNP infusion or by L. farciminis given orally improves TNBS-induced colitis in rats. These results indicate a protective role of NO donation in colonic inflammation and show for the first time a mechanism involving NO delivery by a bacterial strain reducing an experimental colitis.
实验性结肠炎中已报道了乳酸杆菌的有益作用。另一方面,尽管一氧化氮(NO)在肠道炎症过程中的作用存在争议,但已表明外源性NO在炎症中有保护作用。因此,本研究旨在确定(i)NO供体硝普钠(SNP)和(ii)体外产生NO的发酵乳杆菌治疗对三硝基苯磺酸(TNBS)诱导的大鼠结肠炎的影响,并评估外源性NO在此作用中的作用。
将大鼠分为三组,分别接受以下处理之一:(i)连续结肠内(IC)输注SNP 4天,(ii)口服发酵乳杆菌19天,或(iii)生理盐水。分别在第1天和第15天,IC给予TNBS和生理盐水,随后连续IC输注生理盐水或NO清除剂血红蛋白。在治疗结束时,评估以下参数:结肠黏膜的宏观损伤、髓过氧化物酶和一氧化氮合酶活性以及结肠腔内NO产生。
与对照组相比,在结肠炎大鼠中,SNP和发酵乳杆菌治疗显著(P < 0.05)降低了宏观损伤评分、髓过氧化物酶和一氧化氮合酶活性。输注血红蛋白消除了两种NO供体治疗的抗炎作用,但本身对结肠炎无影响。
通过输注SNP或口服发酵乳杆菌在腔内释放的NO可改善TNBS诱导的大鼠结肠炎。这些结果表明NO供体在结肠炎症中具有保护作用,并首次显示了一种机制,即一种细菌菌株通过递送NO减轻实验性结肠炎。