Peran Laura, Camuesco Desiree, Comalada Monica, Nieto Ana, Concha Angel, Adrio José Luis, Olivares Mónica, Xaus Jordi, Zarzuelo Antonio, Galvez Julio
Department of Pharmacology, School of Pharmacy, University of Granada, Campus Universitario La Cartuja s/n, 18071 Granada, Spain.
Int J Colorectal Dis. 2006 Dec;21(8):737-46. doi: 10.1007/s00384-005-0773-y. Epub 2005 Jul 29.
Inflammatory bowel disease is associated with intestinal oxidative stress. In the present study we test the preventative effect of Lactobacillus fermentum, a probiotic that produces per se glutathione, in the trinitrobenzenesulphonic acid (TNBS) model of rat colitis.
Colitis was induced in rats by intracolonic administration of 10 mg of TNBS dissolved in 0.25 ml of 50% ethanol. L. fermentum was administered orally (5x10(8) CFU suspended in 0.5 ml of skim milk) to a group of rats for 3 weeks, starting 2 weeks before colitis induction. Colonic damage was evaluated both histologically and biochemically, and the colonic luminal contents were used for bacterial studies as well as for short chain fatty acid (SCFA) production.
L. fermentum treatment resulted in an amelioration of the inflammatory response in colitic rats as evidenced histologically and by a significant reduction of colonic MPO activity (P<0.05). The probiotic partially counteracted the colonic glutathione depletion induced by the inflammatory process. In addition, probiotic-treated colitic rats showed significant lower colonic tumour necrosis factor (TNF)alpha levels (P<0.01) and inducible nitric oxide synthase (iNOS) expression when compared to non-treated rats. Finally, the probiotic induced growth of Lactobacilli species and production of SCFA in colonic contents in comparison with control colitic rats.
Administration of the probiotic L. fermentum facilitates the recovery of the inflamed tissue in the TNBS model of rat colitis, an effect associated with increased levels of glutathione as well as with amelioration of the production of some of the mediators involved in the inflammatory response of the intestine, such as TNFalpha and NO.
炎症性肠病与肠道氧化应激相关。在本研究中,我们测试了发酵乳杆菌(一种自身能产生谷胱甘肽的益生菌)在大鼠三硝基苯磺酸(TNBS)结肠炎模型中的预防作用。
通过向大鼠结肠内注射溶解于0.25 ml 50%乙醇中的10 mg TNBS诱导结肠炎。一组大鼠在诱导结肠炎前2周开始,口服发酵乳杆菌(5×10⁸CFU悬浮于0.5 ml脱脂乳中),持续3周。从组织学和生物化学方面评估结肠损伤情况,并将结肠腔内容物用于细菌研究以及短链脂肪酸(SCFA)生成的研究。
发酵乳杆菌治疗使结肠炎大鼠的炎症反应得到改善,这在组织学上得到证实,且结肠髓过氧化物酶(MPO)活性显著降低(P<0.05)。该益生菌部分抵消了炎症过程诱导的结肠谷胱甘肽消耗。此外,与未治疗的大鼠相比,经益生菌治疗的结肠炎大鼠结肠肿瘤坏死因子(TNF)α水平显著降低(P<0.01),诱导型一氧化氮合酶(iNOS)表达也降低。最后,与对照结肠炎大鼠相比,该益生菌可诱导结肠内容物中乳酸杆菌属的生长及SCFA的生成。
在大鼠TNBS结肠炎模型中,给予益生菌发酵乳杆菌有助于炎症组织的恢复,这一作用与谷胱甘肽水平升高以及肠道炎症反应中一些介质(如TNFα和NO)生成的改善有关。