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Purification, structural characterization, and cognitive improvement activity of a polysaccharides from Schisandra chinensis

The present study aimed to evaluate structural characteristics of a polysaccharides, SCP2-1, isolated from Schisandra chinensis (Turcz.) Baill (S. chinensis) and to assess its improvement on cognitive dysfunction caused by excessive neuroinflammation. Structural characterization indicated that SCP2-...

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Published in:International journal of biological macromolecules 2020-11, Vol.163, p.497-507
Main Authors: Xu, Mengjie, Yan, Tingxu, Gong, Guowei, Wu, Bo, He, Bosai, Du, Yiyang, Xiao, Feng, Jia, Ying
Format: Article
Language:English
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Summary:The present study aimed to evaluate structural characteristics of a polysaccharides, SCP2-1, isolated from Schisandra chinensis (Turcz.) Baill (S. chinensis) and to assess its improvement on cognitive dysfunction caused by excessive neuroinflammation. Structural characterization indicated that SCP2-1 was composed of glucose and galactose in a molar ratio of 8.78:1.23 with molecular weight of 5.388 kDa. The main linkages of the glycosidic bonds of SCP2-1were 1,4-linked-Glcp, 1,4-linked-Galp, 1-linked-Galp and 1,4,6-linked-Galp. The evaluation of behavioral pharmacology and the detection of biochemical markers exhibited that SCP2-1 could improve LPS-induced cognitive dysfunction in mice, ameliorate excessive inflammatory response. The results showed that SCP2-1 could ameliorated the animals' exploration time of novel arm in Y maze test, shortened the escape latency of mice in MWM test, and increased the exploration time of new object in NOR test. What's more, mice could improve histopathological changes induced by LPS, suppress the over-activation of glial cells, decrease the expression of proinflammatory cytokines, increase the levels of anti-inflammatory cytokines, reduce the levels of NLRP3, M-caspaes-1, which may further induce the decrease of excessive deposition of Aβ. Furthermore, SCP2-1 could inhibit the over-activation of NF-κB and the hyperphosphorylation of P38 MAPK pathway.
ISSN:0141-8130
1879-0003
DOI:10.1016/j.ijbiomac.2020.06.275