Department of Nutrition and Food Hygiene, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Disease, School of Public Health, Soochow University, 199 Renai Road, Suzhou, 215123 Jiangsu, P.R. China.
Independent Scientist, Irving, Texas 75039, United States.
J Agric Food Chem. 2020 Dec 9;68(49):14480-14491. doi: 10.1021/acs.jafc.0c05677. Epub 2020 Nov 25.
It is known that cardiovascular disease can result in cognitive impairment. However, whether oat fiber improves cognitive behavior through a cardiovascular-related mechanism remains unclear. The present work was aimed to elucidate the potential of oat fiber on cognitive behavior by targeting the neuroinflammation signal and microbiome-gut-brain axis in a mouse model of atherosclerosis. Male low-density lipoprotein receptor knock-out (LDLR) mice were treated with a high fat/cholesterol diet without or with 0.8% oat fiber for 14 weeks. Behavioral tests indicated that LDLR mice exhibited a significant cognitive impairment; however, oat fiber can improve cognitive behavior by reducing latency to the platform and increasing the number of crossing and swimming distance in the target quadrant. Oat fiber can inhibit A plaque processing in both the cortex and hippocampus via decreasing the relative protein expression of GFAP and IBα1. Notably, oat fiber inhibited the nod-like receptor family pyrin domain-containing 3 inflammasome activation and blocked the toll-like receptor 4 signal pathway in both the cortex and hippocampus, accompanied by a reduction of circulating serum lipopolysaccharide. In addition, oat fiber raised the expressions of short-chain fatty acid (SCFA) receptors and tight junction proteins (zonula occludens-1 and occludin) and improved intestinal microbiota diversity via increasing the contents of gut metabolites SCFAs. In summary, the present study provided experimental evidence that dietary oat fiber retarded the progression of cognitive impairment in a mouse model of atherosclerosis. Mechanistically, the neuroprotective potential was related to oat fiber and its metabolites SCFAs on the diversity and abundance of gut microbiota that produced anti-inflammatory metabolites, leading to repressed neuroinflammation and reduced gut permeability through the microbiome-gut-brain axis.
已知心血管疾病可导致认知障碍。然而，燕麦纤维是否通过与心血管相关的机制改善认知行为尚不清楚。本研究旨在通过靶向动脉粥样硬化小鼠模型中的神经炎症信号和微生物群-肠-脑轴，阐明燕麦纤维对认知行为的潜在作用。雄性低密度脂蛋白受体敲除（LDLR）小鼠用高脂肪/胆固醇饮食处理，不添加或添加 0.8%的燕麦纤维 14 周。行为测试表明，LDLR 小鼠表现出明显的认知障碍；然而，燕麦纤维可以通过减少到达平台的潜伏期和增加目标象限的穿越和游泳距离来改善认知行为。燕麦纤维可通过降低 GFAP 和 IBα1 的相对蛋白表达来抑制皮质和海马体中的 A 斑块处理。值得注意的是，燕麦纤维抑制了核因子-κB 样受体家族吡咯烷结构域包含蛋白 3 炎性小体的激活，并阻断了皮质和海马体中的 Toll 样受体 4 信号通路，同时循环血清脂多糖减少。此外，燕麦纤维通过增加肠道代谢物短链脂肪酸（SCFA）的含量，提高了短链脂肪酸（SCFA）受体和紧密连接蛋白（闭合蛋白-1 和闭合蛋白）的表达，并改善了肠道微生物群的多样性。总之，本研究为膳食燕麦纤维通过增加肠道代谢物短链脂肪酸（SCFA）的含量，提高了短链脂肪酸（SCFA）受体和紧密连接蛋白（闭合蛋白-1 和闭合蛋白）的表达，并改善了肠道微生物群的多样性。总之，本研究为膳食燕麦纤维通过增加肠道代谢物短链脂肪酸（SCFA）的含量，提高了短链脂肪酸（SCFA）受体和紧密连接蛋白（闭合蛋白-1 和闭合蛋白）的表达，并改善了肠道微生物群的多样性。总之，本研究为膳食燕麦纤维在动脉粥样硬化小鼠模型中延缓认知障碍进展提供了实验依据。从机制上讲，神经保护潜力与燕麦纤维及其代谢物 SCFAs 有关，这些代谢物可改善肠道微生物群的多样性和丰度，产生抗炎代谢物，从而通过微生物群-肠-脑轴抑制神经炎症和减少肠道通透性。
