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岩藻聚糖硫酸酯可改善 LPS 诱导的小鼠神经元细胞损伤和认知障碍。

Fucoidan ameliorates LPS-induced neuronal cell damage and cognitive impairment in mice.

机构信息

School of Life Sciences, Zhengzhou University, Zhengzhou 450001, Henan, China.

NHC Key Laboratory of Birth Defects Prevention, Henan Institute of Reproduction Health Science and Technology, Zhengzhou 450002, Henan, China.

出版信息

Int J Biol Macromol. 2022 Dec 1;222(Pt A):759-771. doi: 10.1016/j.ijbiomac.2022.09.231. Epub 2022 Sep 27.

Abstract

The incidence of cognitive impairment is rising globally, but there is no effective therapy. Recent studies showed that fucoidan (Fuc), a sulfated polysaccharide enriched in brown algae, is widely used due to its anti-inflammatory, antioxidant, and prebiotic effects. However, the effects and mechanisms of Fuc on lipopolysaccharide (LPS)-induced neuronal cell damage and cognitive impairment in mice need to be explored further. In the present study, we found that Fuc treatment protected HT22 cells from LPS-induced damage by inhibiting the activation of NLRP3 inflammasomes. Fuc exerted neuroprotective effects in mice with LPS-induced cognitive impairment by ameliorating neuroinflammation, promoting neurogenesis, and reducing blood-brain barrier and intestinal barrier permeability. Mechanistically, Fuc supplement significantly restructured the gut microbiota composition, which may be related to glucose and fructose metabolism. In conclusion, Fuc ameliorated LPS-induced neuronal cell damage and cognitive impairment in mice, suggesting that Fuc may be a medicinal and food homologous functional agent to improve cognitive function.

摘要

全球认知障碍的发病率正在上升,但目前尚无有效的治疗方法。最近的研究表明,褐藻中富含的硫酸多糖岩藻聚糖(Fuc)具有抗炎、抗氧化和益生元作用,因此被广泛应用。然而,Fuc 对脂多糖(LPS)诱导的神经元细胞损伤和小鼠认知障碍的作用和机制仍需进一步研究。本研究发现,Fuc 通过抑制 NLRP3 炎性小体的激活,可保护 HT22 细胞免受 LPS 诱导的损伤。Fuc 通过改善神经炎症、促进神经发生以及降低血脑屏障和肠道屏障通透性,对 LPS 诱导的认知障碍小鼠发挥神经保护作用。其机制可能与葡萄糖和果糖代谢有关,Fuc 补充剂可显著改变肠道微生物群的组成。总之,Fuc 改善了 LPS 诱导的小鼠神经元细胞损伤和认知障碍,提示 Fuc 可能是一种具有改善认知功能的药食同源功能因子。

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