Abstract：
High-fat and high-fructose diet (HFFD) consumption can induce cognitive dysfunction and gut microbiota disorder. In the present study, the effects of the polysaccharides from the fruits of Lycium barbarum L. (LBPs) on HFFD-induced cognitive deficits and gut microbiota dysbiosis were investigated. The results showed that intervention of LBPs (200 mg/kg/day) for 14 weeks could significantly prevent learning and memory deficits in HFFD-fed mice, evidenced by a reduction of latency and increment of crossing parameters of platform quadrant in Morris water maze test. Moreover, oral administration of LBPs enhanced the expression of postsynaptic density protein 95 and brain-derived neurotrophic factor and reduced the activation of glial cells in hippocampus. Besides, LBPs treatment enriched the relative abundances of Allobaculum and Lactococcus and reduced the relative abundance of Proteobacteria in gut bacterial community of HFFD-fed mice, accompanied by increased levels of short-chain fatty acids (SCFAs) as well as expression of associated G protein-coupled receptors. Furthermore, LBPs intervention prevented insulin resistance, obesity and colonic inflammation. Finally, a significant correlation was observed among neuroinflammation associated parameters, gut microbiota and SCFAs through Pearson correlation analysis. Collectively, these findings suggested that the regulation of gut microbiota might be the potential mechanism of LBPs on preventing cognitive dysfunction induced by HFFD.
摘要：
高脂高果糖饮食(HFFD)可导致认知功能障碍和肠道菌群紊乱。在本研究中,研究了枸杞果实多糖（LBPs）对HFFD引起的认知缺陷和肠道菌群失调的影响。结果表明，LBP（200mg/kg/day）干预14周可以显着预防HFFD喂养小鼠的学习和记忆障碍，在Morris水迷宫测试中，平台象限的延迟减少和穿越参数的增加证明了这一点。此外，口服LBP可增强突触后密度蛋白95和脑源性神经营养因子的表达，并降低海马神经胶质细胞的活化。此外,LBP处理丰富了Allobaculum和乳球菌的相对丰度，并降低了HFFD喂养小鼠的肠道细菌群落中变形杆菌的相对丰度，伴随着短链脂肪酸（SCFA）水平的增加以及相关G蛋白偶联受体的表达。此外，LBP干预可预防胰岛素抵抗，肥胖和结肠炎症。最后,在神经炎症相关参数之间观察到显著的相关性，肠道菌群与SCFA通过Pearson相关性分析。总的来说，这些发现表明，肠道菌群的调节可能是LBP预防HFFD引起的认知功能障碍的潜在机制。
