Shipin Kexue (Apr 2024)

Flammulina velutipes Polysaccharides Alleviate Vascular Inflammation in Mice Exposed to Benzo[a]pyrene via Regulating Myeloid Cytogenesis

  • NIU Zemiao, LI Xin, CHEN Ning, LIANG Zhenhua, ZHAO Juan, LÜ Pin, ZHANG Yan, FU Chenghao

DOI
https://doi.org/10.7506/spkx1002-6630-20230628-225
Journal volume & issue
Vol. 45, no. 8
pp. 105 – 113

Abstract

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Flammulina velutipes polysaccharides (FVP) have been reported to exhibit excellent anti-inflammatory and antioxidant effects. This study further investigated the efficacy and mechanism of action of FVP in alleviating vascular injury induced by benzo[a]pyrene (BaP) in mice. The expression of vascular inflammatory cytokines was assessed through immunohistochemistry analysis. Flow cytometry was used to analyze the proportion of pro-inflammatory cells in the peripheral blood and spleen as well as the composition of hematopoietic stem cell (HSC) subsets in bone marrow. The results demonstrated that FVP treatment mitigated the expression of vascular pro-inflammatory cytokines such as interleukin-6, monocyte chemoattractant protein-1 and intercellular cell adhesion molecule-1 in mice induced by BaP. Moreover, FVP treatment significantly inhibited the increases in the proportions of monocytes, macrophages and neutrophils in the peripheral blood and those of macrophages and neutrophils in the spleen of BaP-induced mice. Further analysis of bone marrow HSC subsets revealed that BaP exposure elevated the proportions of hematopoietic progenitor cells and granulocyte-macrophage progenitor cells in mouse bone marrow, while reducing the proportions of hematopoietic stem cells and common myeloid progenitor cells, which were reversed by FVP treatment, thus restoring bone marrow HSC subsets to the level of the healthy control group. At the cellular level, FVP suppressed BaP-induced oxidative stress in Raw264.7 cells. Taken together, FVP alleviate BaP-induced vascular inflammatory injury by maintaining the homeostasis of the bone marrow hematopoietic system, thereby regulating the output of pro-inflammatory cells into the circulatory system, and down-regulating the proportion of peripheral pro-inflammatory cells.

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