a Department of Molecular Medicine , Qazvin University of Medical Sciences , Qazvin , Iran.
b NeuroBiology Research Center , Shahid Beheshti University of Medical Sciences , Tehran , Iran.
J Am Coll Nutr. 2019 Mar-Apr;38(3):209-217. doi: 10.1080/07315724.2018.1487346. Epub 2018 Oct 11.
The role of gut microbiota in the pathogenesis of several neurodegenerative disorders, including Alzheimer's disease (AD), via the gut-brain axis has recently been demonstrated; hence, modification of the intestinal microbiota composition by probiotic biotherapy could be a therapeutic target for these conditions. The aim of this study was to assess the effects of a probiotic formulation (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) on inflammatory and memory processes in lipopolysaccharide (LPS)-induced rats, one of the animal models used in peripherally induced neuroinflammation and neurodegeneration.
Rats were randomly divided into four groups (Control, LPS, Probiotic + LPS, and Probiotic). All experimental groups were orally administrated maltodextrin (placebo) or probiotic (10 CFU/ml/rat) for 14 consecutive days and then were injected with saline or LPS (1 mg/kg, intraperitoneally [i.p.], single dose) 20 hours later. Memory retention ability and systemic and neuroinflammatory markers were assessed 4 hours after the injections.
Systemic exposure to LPS resulted in significant elevation of both the circulating and hippocampal levels of proinflammatory cytokines, which decreased remarkably following probiotic pretreatment. Oral bacteriotherapy with a combination of L. helveticus R0052 and B. longum R0175 also attenuated the decremental effect of LPS on memory through brain-derived neurotrophic factor (BDNF) expression at the molecular level; however, this effect was not significant in the passive avoidance test at the behavioral level.
These results suggest that the management of gut microbiota with this probiotic formulation could be a promising intervention to improve neuroinflammation-associated disorders such as AD.
通过肠-脑轴，肠道微生物群在包括阿尔茨海默病（AD）在内的几种神经退行性疾病的发病机制中发挥作用，最近已经得到证实；因此，通过益生菌生物疗法来改变肠道微生物群的组成可能是这些疾病的治疗靶点。本研究旨在评估益生菌制剂（瑞士乳杆菌 R0052 和长双歧杆菌 R0175）对脂多糖（LPS）诱导的大鼠炎症和记忆过程的影响，LPS 诱导的大鼠是外周诱导的神经炎症和神经退行性变的动物模型之一。
大鼠随机分为四组（对照组、LPS 组、益生菌+LPS 组和益生菌组）。所有实验组连续 14 天口服麦芽糖糊精（安慰剂）或益生菌（10 CFU/ml/大鼠），然后 20 小时后腹腔内（i.p.）注射生理盐水或 LPS（1mg/kg，单次剂量）。注射后 4 小时评估记忆保留能力和全身及神经炎症标志物。
全身暴露于 LPS 导致循环和海马中促炎细胞因子水平显著升高，而益生菌预处理后明显降低。瑞士乳杆菌 R0052 和长双歧杆菌 R0175 的联合口服细菌疗法也通过脑源性神经营养因子（BDNF）表达在分子水平上减弱了 LPS 对记忆的递减作用；然而，在行为水平的被动回避测试中，这种作用并不显著。
这些结果表明，用这种益生菌制剂来管理肠道微生物群可能是改善与神经炎症相关的疾病（如 AD）的一种有前途的干预措施。
