Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogen Biology and Immunology, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, China.
Electron Microscope Unit, Mark Wainwright Analytical Centre, The University of New South Wales, Sydney, NSW, 2052, Australia.
J Transl Med. 2021 Feb 4;19(1):54. doi: 10.1186/s12967-021-02724-6.
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.
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功能下降。（1，3）/（1，6）-β-葡聚糖是一种从药用蘑菇香菇（Lentinula edodes）中分离出来的可食用多糖，具有重塑肠道微生物群的潜力。然而，香菇衍生的β-葡聚糖对 HF 饮食诱导的神经炎症和认知功能下降的影响尚不清楚。本研究旨在评估膳食香菇β-葡聚糖补充剂对 HF 饮食喂养的肥胖相关认知功能下降的小鼠的神经保护作用及其机制。
C57BL/6J 雄性小鼠分别用实验室标准饲料（LC）、HF 或 HF 加香菇β-葡聚糖补充剂喂养 7 天（短期）或 15 周（长期）。评估代谢参数、内毒素、肠道微生物群、结肠和大脑病理变化；采集血液、盲肠内容物、结肠和大脑，检测认知行为。
我们报道，香菇β-葡聚糖的短期和长期补充可防止 HF 饮食引起的肠道微生物组成变化。长期香菇β-葡聚糖补充可防止 HF 饮食诱导的行为测试（时序记忆、新物体识别和 Y 迷宫测试）引起的识别记忆障碍。在大脑前额叶皮层和海马体中，β-葡聚糖补充可改善 HF 饮食引起的突触超微结构、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 HF 饮食喂养的小鼠结肠的黏膜厚度，上调了紧密连接蛋白 occludin 的表达，降低了血浆 LPS 水平，并抑制了促炎巨噬细胞在结肠中的聚集。
本研究表明，香菇β-葡聚糖可预防 HF 饮食引起的认知障碍，其可能通过改善结肠-脑轴发生。该研究结果表明，膳食香菇β-葡聚糖补充可能是预防肥胖相关认知功能下降的有效营养策略。
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