β-Glucan from Lentinula edodes prevents cognitive impairments in high-fat diet-induced obese mice: involvement of colon-brain axis.

β-Glucan from Lentinula edodes prevents cognitive impairments in high-fat diet-induced obese mice: involvement of colon-brain axis.
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香菇中的β-葡聚糖可预防高脂饮食引起的肥胖小鼠的认知障碍:涉及结肠-脑轴

DOI:
10.1186/s12967-021-02724-6
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发表时间:
2021-02-04
影响因子:
7.4
通讯作者:
Yu Y
Yu Y
中科院分区:
医学2区
文献类型:
--
作者:
Pan W;Jiang P;Zhao J;Shi H;Zhang P;Yang X;Biazik J;Hu M;Hua H;Ge X;Huang XF;Yu Y

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长期高脂肪(HF)饮食摄入可通过肠-脑轴引起神经炎症和认知能力下降。(1,3)/(1,6)-β-葡聚糖是从药用蘑菇香菇(Lentinula edodes(L. edodes),具有重塑肠道微生物群的潜力。但L.香菇衍生的β-葡聚糖对HF饮食诱导的神经炎症和认知能力下降的作用仍然未知。本研究旨在评估膳食补充香菇β-葡聚糖对HF饮食喂养小鼠肥胖相关认知能力下降的神经保护作用和机制。C57 BL/6 J雄性小鼠喂食实验室食物(LC)、HF或HF与L. edodes β-葡聚糖补充饮食7天(短期)或15周(长期)。检查认知行为;收集血液、盲肠内容物、结肠和脑以评价代谢参数、内毒素、肠道微生物群、结肠和脑病理学。我们报道了短期和长期L。香菇β-葡聚糖补充剂可防止HF饮食诱导的肠道微生物组成变化。长期湖通过行为测试(时间顺序记忆、新物体识别和Y-迷宫测试)评估,edodes β-葡聚糖补充剂可预防HF饮食诱导的识别记忆障碍。在前额叶皮层和海马中,β-葡聚糖补充剂改善了HF饮食诱导的突触超微结构、神经炎症和脑源性神经营养因子(BDNF)缺陷的改变。此外,β-葡聚糖补充增加了粘膜厚度,上调了紧密连接蛋白occludin的表达,降低了血浆LPS水平,并抑制了HF饮食喂养小鼠结肠中促炎性巨噬细胞的积聚。本研究揭示了L. edodes β-葡聚糖可预防HF饮食引起的认知障碍,这可能通过改善结肠-脑轴而发生。这一发现表明,膳食L。edodes β-葡聚糖补充剂可能是预防肥胖相关认知能力下降的有效营养策略。
Long-term high fat (HF) diet intake can cause neuroinflammation and cognitive decline through the gut-brain axis. (1, 3)/(1, 6)-β-glucan, an edible polysaccharide isolated from medical mushroom, Lentinula edodes (L. edodes), has the potential to remodel gut microbiota. However, the effects of L. edodes derived β-glucan against HF diet-induced neuroinflammation and cognitive decline remain unknown. This study aimed to evaluate the neuroprotective effect and mechanism of dietary L edodes β-glucan supplementation against the obesity-associated cognitive decline in mice fed by a HF diet. C57BL/6J male mice were fed with either a lab chow (LC), HF or HF with L. edodes β-glucan supplementation diets for 7 days (short-term) or 15 weeks (long-term). Cognitive behavior was examined; blood, cecum content, colon and brain were collected to evaluate metabolic parameters, endotoxin, gut microbiota, colon, and brain pathology. We reported that short-term and long-term L. edodes β-glucan supplementation prevented the gut microbial composition shift induced by the HF diet. Long-term L. edodes β-glucan supplementation prevented the HF diet-induced recognition memory impairment assessed by behavioral tests (the temporal order memory, novel object recognition and Y-maze tests). In the prefrontal cortex and hippocampus, the β-glucan supplementation ameliorated the alteration of synaptic ultrastructure, neuroinflammation and brain-derived neurotrophic factor (BDNF) deficits induced by HF diet. Furthermore, the β-glucan supplementation increased the mucosal thickness, upregulated the expression of tight junction protein occludin, decreased the plasma LPS level, and inhibited the proinflammatory macrophage accumulation in the colon of mice fed by HF diet. This study revealed that L. edodes β-glucan prevents cognitive impairments induced by the HF diet, which may occur via colon-brain axis improvement. The finding suggested that dietary L. edodes β-glucan supplementation may be an effective nutritional strategy to prevent obesity-associated cognitive decline.
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发表时间: 2007-07-01
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