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益生菌通过逆转肠道菌群异常发挥对脓毒症诱导认知障碍的保护作用。

Probiotics Exert Protective Effect against Sepsis-Induced Cognitive Impairment by Reversing Gut Microbiota Abnormalities.

机构信息

Department of Neurology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China.

Department of Preventive Medicine, School of Public Health and Management, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.

出版信息

J Agric Food Chem. 2020 Dec 16;68(50):14874-14883. doi: 10.1021/acs.jafc.0c06332. Epub 2020 Dec 7.

DOI:10.1021/acs.jafc.0c06332
PMID:33284020
Abstract

Recent evidence has revealed that probiotics could affect neurodevelopment and cognitive function via regulating gut microbiota. However, the role of probiotics in sepsis-associated encephalopathy (SAE) remained unclear. This study was conducted to assess the effects and therapeutic mechanisms of probiotic (Cb) against SAE in mice. The SAE model mouse was induced by cecal ligation and puncture (CLP) and was given by intragastric administration with Cb for 1 month. A series of behavioral tests, including neurological severity score, tail suspension test, and elevated maze test, were used to assess cognitive impairment. Nissl staining and Fluoro-Jade C (FJC) staining were used to assess neuronal injury. Microglia activation, the release of neuroinflammatory cytokines, and the levels of ionized calcium-binding adapter molecule 1 (Iba-1) and brain-derived neurotrophic factor (BDNF) in the brain were determined. The compositions of the gut microbiota were detected by 16S rRNA sequencing. Our results revealed that Cb significantly attenuated cognitive impairment and neuronal damage. Moreover, Cb significantly inhibited excessive activation of microglia, decreased Iba-1 level, and increased BDNF level in the SAE mice. In addition, Cb improved gut microbiota dysbiosis of SAE mice. These findings revealed that Cb exerted anti-inflammatory effects and improved cognitive impairment in SAE mice, and their neuroprotective mechanisms might be mediated by regulating gut microbiota.

摘要

最近的证据表明,益生菌可以通过调节肠道微生物群来影响神经发育和认知功能。然而,益生菌在脓毒症相关性脑病(SAE)中的作用尚不清楚。本研究旨在评估益生菌(Cb)对小鼠 SAE 的作用及其治疗机制。通过盲肠结扎和穿刺(CLP)诱导 SAE 模型小鼠,并通过灌胃给予 Cb 1 个月。一系列行为测试,包括神经严重程度评分、悬尾试验和高架迷宫试验,用于评估认知障碍。尼氏染色和氟代-Jade C(FJC)染色用于评估神经元损伤。测定小胶质细胞激活、神经炎症细胞因子释放以及脑内离子钙结合接头蛋白 1(Iba-1)和脑源性神经营养因子(BDNF)水平。通过 16S rRNA 测序检测肠道微生物群的组成。我们的结果表明,Cb 显著减轻了认知障碍和神经元损伤。此外,Cb 显著抑制了 SAE 小鼠小胶质细胞的过度激活,降低了 Iba-1 水平,并增加了 BDNF 水平。此外,Cb 改善了 SAE 小鼠的肠道微生物群失调。这些发现表明 Cb 在 SAE 小鼠中发挥抗炎作用并改善认知障碍,其神经保护机制可能通过调节肠道微生物群来介导。

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