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发酵褐藻糖胶和 λ-卡拉胶通过调节肠道微生物群及其在海马淀粉样 β 输注大鼠中的宏基因组功能来减轻记忆障碍。

Mitigation of Memory Impairment with Fermented Fucoidan and λ-Carrageenan Supplementation through Modulating the Gut Microbiota and Their Metagenome Function in Hippocampal Amyloid-β Infused Rats.

机构信息

Department of Bioconvergence System, Hoseo University, Asan 31499, Korea.

Department of Food and Nutrition, Obesity/Diabetes Research Center, Hoseo University, Asan 31499, Korea.

出版信息

Cells. 2022 Jul 26;11(15):2301. doi: 10.3390/cells11152301.

DOI:10.3390/cells11152301
PMID:35892598
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9367263/
Abstract

Attenuating acetylcholinesterase and insulin/insulin-like growth factor-1 signaling in the hippocampus is associated with Alzheimer's disease (AD) development. Fucoidan and carrageenan are brown and red algae, respectively, with potent antibacterial, anti-inflammatory, antioxidant and antiviral activities. This study examined how low-molecular-weight (MW) and high-MW fucoidan and λ-carrageenan would improve memory impairment in Alzheimer's disease-induced rats caused by an infusion of toxic amyloid-β(Aβ). Fucoidan and λ-carrageenan were dissected into low-MW by   and  . Rats receiving an Aβ(25-35) infusion in the CA1 region of the hippocampus were fed dextrin (AD-Con), 1% high-MW fucoidan (AD-F-H), 1% low-MW fucoidan (AD-F-L), 1% high-MW λ-carrageenan (AD-C-H), and 1% low-MW λ-carrageenan (AD-C-L) for six weeks. Rats to receive saline infusion (Normal-Con) had an AD-Con diet. The AD-F-L group showed an improved memory function, which manifested as an enhanced Y-maze spontaneous alternation test, water maze, and passive avoidance tests, similar to the Normal-Con group. AD-F-L also potentiated hippocampal insulin signaling and increased the expression of ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF) in the hippocampus. AD-C-L improved the memory function mainly by increasing the BDNF content. AD-F-H and AD-C-H did not improve the memory function. Compared to AD-Con, the ascending order of AD-C-H, AD-F-H, AD-C-L, and AD-F-L increased insulin signaling by enhancing the pSTAT3®pAkt®pGSK-3β pathway. AD-F-L improved glucose tolerance the most. Compared to AD-CON, the AD-F-L treatment increased the serum acetate concentrations and compensated for the defect of cerebral glucose metabolism. AD-Con increased , and compared to Normal-Con, and AD-F-L and AD-C-L increased . In conclusion, AD-F-L and AD-C-L alleviated the memory function in the rats with induced AD symptoms by modulating.

摘要

乙酰胆碱酯酶和胰岛素/胰岛素样生长因子-1 信号在海马中的衰减与阿尔茨海默病 (AD) 的发展有关。褐藻糖胶和角叉菜胶分别是棕色和红色藻类,具有强大的抗菌、抗炎、抗氧化和抗病毒活性。本研究探讨了低分子量 (MW) 和高分子量 (MW) 褐藻糖胶和 λ-角叉菜胶如何改善由有毒淀粉样蛋白-β (Aβ) 输注引起的阿尔茨海默病诱导大鼠的记忆障碍。褐藻糖胶和 λ-角叉菜胶通过   和   被分离成低分子量。在海马 CA1 区接受 Aβ(25-35) 输注的大鼠喂食糊精 (AD-Con)、1%高分子量褐藻糖胶 (AD-F-H)、1%低分子量褐藻糖胶 (AD-F-L)、1%高分子量 λ-角叉菜胶 (AD-C-H) 和 1%低分子量 λ-角叉菜胶 (AD-C-L) 六周。接受盐水输注的大鼠 (正常对照) 给予 AD-Con 饮食。AD-F-L 组表现出改善的记忆功能,这表现为 Y 迷宫自发交替测试、水迷宫和被动回避测试的增强,类似于正常对照。AD-F-L 还增强了海马胰岛素信号,并增加了海马中的睫状神经营养因子 (CNTF) 和脑源性神经营养因子 (BDNF) 的表达。AD-C-L 主要通过增加 BDNF 含量来改善记忆功能。AD-F-H 和 AD-C-H 均未改善记忆功能。与 AD-Con 相比,AD-C-H、AD-F-H、AD-C-L 和 AD-F-L 的胰岛素信号呈上升趋势,通过增强 pSTAT3®pAkt®pGSK-3β 途径增强。AD-F-L 改善葡萄糖耐量的效果最为明显。与 AD-Con 相比,AD-F-L 治疗增加了血清乙酸盐浓度,并补偿了大脑葡萄糖代谢的缺陷。AD-Con 与 Normal-Con 相比增加了  、  和  ,而 AD-F-L 和 AD-C-L 增加了  。总之,AD-F-L 和 AD-C-L 通过调节 ,缓解了具有诱导 AD 症状大鼠的记忆功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/7aceec16c3da/cells-11-02301-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/817a6db73106/cells-11-02301-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/7799bd8e9e6b/cells-11-02301-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/1ac3e94f8a35/cells-11-02301-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/57e5b7592207/cells-11-02301-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/ea96d7912c15/cells-11-02301-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/7aceec16c3da/cells-11-02301-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/817a6db73106/cells-11-02301-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/7799bd8e9e6b/cells-11-02301-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/1ac3e94f8a35/cells-11-02301-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/57e5b7592207/cells-11-02301-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/ea96d7912c15/cells-11-02301-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcd4/9367263/7aceec16c3da/cells-11-02301-g006a.jpg

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