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Bifidobacterium pseudocatenulatum CECT 7765 supplementation restores altered vascular function in an experimental model of obese mice

机译:伪双歧杆菌CECT 7765补充剂可恢复肥胖小鼠实验模型中血管功能的改变

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>Aims. Bifidobacterium pseudocatenulatum CECT 7765 improves metabolic and immunological altered functions in high fat fed mice, however little is known about the effects of potential probiotics on vascular reactivity. The aim of the present study was to investigate the effects of a potential probiotic strain, Bifidobacterium pseudocatenulatum CECT 7765, on vascular response in obese mice.>Methods. Aorta samples were obtained from mice, which were divided into three groups: a control group, receiving a standard diet; an obese group, receiving a high-fat diet; and an obese group receiving high-fat diet and a daily dose of B. pseudocatenulatum CECT 7765 by oral gavage. Aortic rings were suspended in organ baths for isometric recording of tension. mRNA expression of eNOS was evaluated by real-time polymerase chain reaction.>Results. Contractions induced by KCl, noradrenaline and thromboxane analogue were 33%, 30% and 45% lower respectively in aortic rings from obese mice. Bifidobacteria administration reversed this effect. eNOS inhibition increased the response to noradrenaline in the three groups with a significant lower magnitude in aortic rings from obese mice receiving bifidobacteria supplement. Acetylcholine caused a greater vasodilation in aorta from obese group (46±3% for control and 69±4% for obese group; p<0.05) and bifidobacteria reversed it (57±5%). Response to sodium nitroprusside was displaced 2.9 times to the left in a parallel manner in obese group. Relaxation to sodium nitroprusside remained unchanged in the bifidobacteria fed group. There was about five-fold decreased mRNA expression of eNOS in aortic segments from the group receiving bifidobacteria.>Conclusion. Bifidobacterium pseudocatenulatum CECT 7765 restores the obesity-induced altered vascular function mainly by reducing nitric oxide release.
机译:>目的。伪双歧杆菌CECT 7765可以改善高脂喂养小鼠的代谢和免疫功能改变,但对潜在益生菌对血管反应性的影响知之甚少。本研究的目的是研究潜在的益生菌菌株假双歧杆菌CECT 7765对肥胖小鼠血管反应的影响。>方法。 从小鼠中获得主动脉样品,将其分为三组:对照组,接受标准饮食;对照组,接受常规饮食。接受高脂饮食的肥胖人群;以及通过口服管饲法接受每日高脂饮食和每日剂量假性链球菌CECT 7765的肥胖人群。将主动脉环悬挂在器官浴中,以等距记录张力。通过实时聚合酶链反应评估eNOS的mRNA表达。>结果。 在肥胖小鼠的主动脉环中,氯化钾,去甲肾上腺素和血栓烷类似物引起的收缩分别降低33%,30%和45%。双歧杆菌给药逆转了这种作用。 eNOS抑制在三组中增加了对接受去甲肾上腺素的反应,而肥胖小鼠接受双歧杆菌补充后的主动脉环幅度明显降低。乙酰胆碱使肥胖组的主动脉血管扩张更大(对照组为46±3%,肥胖组为69±4%; p <0.05),双歧杆菌逆转了(57±5%)。在肥胖组中,对硝普钠的反应以平行的方式向左移位了2.9倍。双歧杆菌喂养组对硝普钠的松弛保持不变。接受双歧杆菌组的主动脉节段中eNOS的mRNA表达降低了约五倍。>结论。伪双歧杆菌CECT 7765主要通过减少一氧化氮的释放来恢复肥胖引起的血管功能改变。

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