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- Title
广叶绣球菌多糖对免疫低下小鼠海马组织cAMP-PKA-CREB-BDNF信号通路的影响.
- Authors
阮进基; 谢添; 云少君; 程艳芬; 曹谨玲; 程菲儿; 冯翠萍
- Abstract
The effects of Sparassis latifolia polysaccharides (SCPs) on cAMP-PKA-CREB-BDNF signaling pathway in cyclophosphamide-induced immunosuppressed mice were explored. The immunosuppressed mice were administered SCPs by gavage feeding at 100 mg·kg-1 (LD), 200 mg·kg-1 (MD) and 400 mg·kg-1 (HD), respectively. For each group, SCPs were evaluated for protective effects on hippocampal tissue injury in terms of morphological changes of hippocampus, contents of 5-hydroxytryptamine (5-HT), tryptophan hydroxylase 2 (TPH2) and cyclic adenosine monophosphate (cAMP), mRNA levels of cytokinis and genes in cAMP-PKA-CREB-BDNF signaling pathway, and protein levels of cAMP response element binding protein (CREB) and phosphorylated CREB (p-CREB). The results showed that SCPs increased the number of hippocampal nerve cells and reduced the intercelluar space to make a more complete tissue structure in immunosuppressed mice (model group). Compared with the model group, both 5-HT and TPH2 were extremely significantly (P<0.01) increased in all three SCPs groups, and cAMP was extremely significantly (P<0.01) increased in MD and HD. In contrast, TNF-α mRNA was significantly decreased in all three SCPs groups, and IL-1β mRNA was decreased in MD and HD. There was a significant increase of 5-HT1A receptor gene mRNA in MD and HD, and a significant increase of both PKA mRNA and BDNF mRNA in HD compared with the model group. There was a significant increase of CREB protein level in HD and a signficant increase of p-CREB in all three SCPs groups. These findings provided a reference for revealing the underlying mechanism of the protective effects of SCPs on cyclophosphamide-induced hippocampal damages.
- Subjects
CYCLIC adenylic acid; TRYPTOPHAN hydroxylase; CREB protein; NEURONS; CARRIER proteins; THETA rhythm; HIPPOCAMPUS (Brain)
- Publication
Acta Edulis Fungi, 2022, Vol 29, Issue 1, p66
- ISSN
1005-9873
- Publication type
Article
- DOI
10.16488/j.cnki.1005-9873.2022.01.009