4.7 Article

Dietary Supplement of Anoectochilus roxburghii (Wall.) Lindl. Polysaccharides Ameliorates Cognitive Dysfunction Induced by High Fat Diet via Gut-Brain Axis

期刊

DRUG DESIGN DEVELOPMENT AND THERAPY
卷 16, 期 -, 页码 1931-1945

出版社

DOVE MEDICAL PRESS LTD
DOI: 10.2147/DDDT.S356934

关键词

Anoectochilus roxburghii (Wall; ) Lindl; polysaccharides; diet-induced-obesity; cognitive dysfunction; gut microbiota; ?gut-brain? axis

资金

  1. Science and Technology Planning Project of Sichuan Province [2019YFS0180]
  2. Doctoral Research Initiation Fund of Affiliated Hospital of Southwest Medical University [21032]
  3. Collaborative Project of Luzhou Government and Southwest Medical University [2018LZXNYDPT02]
  4. Foundation for Young Scholars of Southwest Medical University [2019-ZQN-125, 2020-ZQN-151]

向作者/读者索取更多资源

This study found that ARPs can improve cognitive dysfunction induced by HFD by reducing the phosphorylation levels of Tau protein in the hippocampus, lowering body weight, blood glucose and cholesterol levels, and reducing inflammatory factors. In addition, ARPs also exert their effects by restoring intestinal barrier integrity and regulating gut microbiota.
Purpose: Anoectochilus roxburghii (Wall.) Lindl. polysaccharides (ARPs) have been reported to exhibit multiple pharmacological activities including anti-inflammatory and anti-hyperglycemia. This study aims to investigate the effect of ARPs on cognitive dysfunction induced by high fat diet (HFD). Methods: Six-week-old male mice were treated with ARPs by dietary supplementation for 14 weeks. The effect of ARPs on cognitive function was determined by assessing the changes in spatial learning and memory ability, neurotrophic factors in hippocampus, inflammatory parameters, intestinal barrier integrity, and gut microbiota. Results: ARPs supplementation can effectively ameliorate cognitive dysfunction, decrease the phosphorylation levels of Tau protein in hippocampus. Meanwhile, the increased body weight, plasma glucose, total cholesterol, inflammatory factors induced by HFD were abolished by ARPs treatment. Furthermore, ARPs treatment restored the intestinal epithelial barrier as evidenced by upregulation of intestinal tight junction proteins. Additionally, ARPs supplementation significantly decreased the relative abundance of several bacteria genus such as Parabacteroides, which may play regulatory roles in cognitive function. Conclusion: These results suggest that ARPs might be a promising strategy for the treatment of cognitive dysfunction induced by HFD. Mechanistically, alleviation of cognitive dysfunction by ARPs might be associated with the ???gut-brain??? axis.

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