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

机译:在小鼠败血症性休克实验模型中评价发酵乳杆菌的预防作用

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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.
机译:在小鼠败血性休克的脂多糖(LPS)模型中评估了益生菌发酵乳杆菌CECT5716的预防作用。益生菌悬浮于饮用水中,最终浓度为108个菌落形成单位/ ml,持续2周,然后通过腹膜内注射LPS(每只小鼠400微克/ 200微升)诱导内毒素休克。 24小时后收集血液和不同器官,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的TNF-α水平,从而促进了败血性休克期间观察到的主要变化以及活化的中性粒细胞浸润到肺中。此外,自由基过度产生和氧化应激与败血性小鼠肝谷胱甘肽水平的显着降低有关,并且归因于诱导型NO合酶(iNOS)诱导型的过量NO产生。实际上,在接受益生菌的那组小鼠中肝谷胱甘肽水平显着增加,而用发酵乳杆菌治疗的那些小鼠在结肠和肺中iNOS表达的增加均被下调。最后,用发酵乳杆菌预处理还可以发挥其保护作用,调节脾细胞衍生的T细胞(例如IL-2,IL-5,IL-6或IL-10)中不同细胞因子的表达。总之,用发酵乳杆菌的预处理可能通过结合多种作用(包括其抗氧化特性)和减少促炎性TNF-α和IL-的合成来发挥其对LPS诱导的小鼠器官损伤的保护作用。 6。

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