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在小鼠脓毒症休克实验模型中对发酵乳杆菌发挥的预防作用进行评估。

Evaluation of the preventative effects exerted by Lactobacillus fermentum in an experimental model of septic shock induced in mice.

作者信息

Arribas Belén, Rodríguez-Cabezas Maria Elena, Comalada Mònica, Bailón Elvira, Camuesco Desireé, Olivares Mónica, Xaus Jordi, Zarzuelo Antonio, Gálvez Julio

机构信息

Department of Pharmacology, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, University of Granada, Granada, Spain.

出版信息

Br J Nutr. 2009 Jan;101(1):51-8. doi: 10.1017/S0007114508986876. Epub 2008 Apr 29.

DOI:10.1017/S0007114508986876
PMID:18445307
Abstract

The preventative effects of the probiotic Lactobacillus fermentum CECT5716 were evaluated in the lipopolysaccharide (LPS) model of septic shock in mice. The probiotic was administered suspended in drinking water at the final concentration of 108 colony-forming units/ml for 2 weeks before the induction of an endotoxic shock by an intraperitoneal injection of LPS (400 microg/200 microl per mouse). Blood and different organs were collected after 24 h to evaluate the severity of the endotoxic shock and the preventative effects of the probiotic. L. fermentum reduced TNF-alpha levels in blood, which promotes the major alterations observed during septic shock, as well as the infiltration of activated neutrophils into the lungs. Furthermore, free radical overproduction and oxidative stress were associated with a significant decrease in hepatic glutathione levels in septic mice, and with an excessive NO production attributed to the induction of the inducible isoform of NO synthase (iNOS). In fact, hepatic glutathione levels were significantly increased in the group of mice receiving the probiotic, and the increased iNOS expression both in the colon and lungs was down-regulated in those mice treated with L. fermentum. Finally, pre-treatment with L. fermentum may also exert its protective action modulating the expression of different cytokines in splenocyte-derived T cells such us IL-2, IL-5, IL-6 or IL-10. In conclusion, pre-treatment with L. fermentum may exert its protective action against LPS-induced organ damage in mice by a combination of several actions including its antioxidant properties and by reduction of the synthesis of the pro-inflammatory TNF-alpha and IL-6.

摘要

在小鼠脓毒性休克的脂多糖(LPS)模型中评估了益生菌发酵乳杆菌CECT5716的预防作用。在通过腹腔注射LPS(每只小鼠400微克/200微升)诱导内毒素休克前2周,将益生菌悬浮于饮用水中,以终浓度10⁸ 菌落形成单位/毫升给药。24小时后采集血液和不同器官,以评估内毒素休克的严重程度和益生菌的预防作用。发酵乳杆菌降低了血液中TNF-α水平,TNF-α会促进脓毒性休克期间观察到的主要变化,以及活化中性粒细胞向肺部的浸润。此外,自由基过量产生和氧化应激与脓毒症小鼠肝脏谷胱甘肽水平显著降低以及诱导型一氧化氮合酶(iNOS)诱导导致的过量一氧化氮产生有关。事实上,接受益生菌的小鼠组肝脏谷胱甘肽水平显著升高,并且在接受发酵乳杆菌治疗的小鼠中,结肠和肺部iNOS表达的增加均被下调。最后,用发酵乳杆菌预处理还可能通过调节脾细胞来源的T细胞中不同细胞因子(如IL-2、IL-5、IL-6或IL-10)的表达发挥其保护作用。总之,用发酵乳杆菌预处理可能通过多种作用的组合,包括其抗氧化特性以及减少促炎细胞因子TNF-α和IL-6的合成,对小鼠LPS诱导的器官损伤发挥保护作用。

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