Department of Histology and Embryology, Guangdong Medical University, Zhanjiang, China.
Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute of Neurology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
J Alzheimers Dis. 2020;77(2):629-640. doi: 10.3233/JAD-200035.
Excessive salt intake is considered as an important risk factor for cognitive impairment, which might be the consequence of imbalanced intestinal homeostasis.
To investigate the effects of dietary salt on the gut microbiota and cognitive performance and the underlying mechanisms.
Adult female C57BL/6 mice were maintained on either normal chow (control group, CON) or sodium-rich chow containing 8% NaCl (high-salt diet, HSD) for 8 weeks. Spatial learning and memory ability, short-chain fatty acids (SCFAs) concentrations, gut bacterial flora composition, blood-brain barrier permeability, and proinflammatory cytokine levels and apoptosis in the brain were evaluated.
The mice fed a HSD for 8 weeks displayed impaired learning and memory abilities. HSD significantly reduced the proportions of Bacteroidetes (S24-7 and Alloprevotella) and Proteobacteria and increased that of Firmicutes (Lachnospiraceae and Ruminococcaceae). SCFA concentrations decreased in the absolute concentrations of acetate, propionate, and butyrate in the fecal samples from the HSD-fed mice. The HSD induced both BBB dysfunction and microglial activation in the mouse brain, and increased the IL-1β, IL-6, and TNF-α expression levels in the cortex. More importantly, the degree of apoptosis was higher in the cortex and hippocampus region of mice fed the HSD, and this effect was accompanied by significantly higher expression of cleaved caspase-3, caspase-3, and caspase-1.
The HSD directly causes cognitive dysfunction in mice by eliciting an inflammatory environment and triggering apoptosis in the brain, and these effects are accompanied by gut dysbiosis, particularly reduced SCFA production.
过量摄入盐被认为是认知障碍的一个重要危险因素，其可能是肠道内环境失衡的结果。
研究饮食盐对肠道微生物群和认知功能的影响及其潜在机制。
将成年雌性 C57BL/6 小鼠维持在正常饲料（对照组，CON）或含 8%NaCl 的高盐饮食（HSD）中 8 周。评估空间学习和记忆能力、短链脂肪酸（SCFAs）浓度、肠道细菌群落组成、血脑屏障通透性以及大脑中的促炎细胞因子水平和细胞凋亡情况。
8 周 HSD 喂养的小鼠表现出学习和记忆能力受损。HSD 显著降低了拟杆菌门（S24-7 和 Alloprevotella）和变形菌门的比例，增加了厚壁菌门（Lachnospiraceae 和 Ruminococcaceae）的比例。HSD 喂养小鼠粪便中 SCFA 浓度绝对浓度的乙酸、丙酸和丁酸均降低。HSD 诱导了小鼠大脑中血脑屏障功能障碍和小胶质细胞激活，并增加了皮质中 IL-1β、IL-6 和 TNF-α的表达水平。更重要的是，HSD 喂养的小鼠皮质和海马区的细胞凋亡程度更高，并且伴随着 cleaved caspase-3、caspase-3 和 caspase-1 的表达显著升高。
HSD 通过引发炎症环境和触发大脑细胞凋亡，直接导致小鼠认知功能障碍，而这些影响伴随着肠道菌群失调，特别是 SCFA 产生减少。
