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. 2020 Jul 7;247:116740. doi: 10.1016/j.carbpol.2020.116740

Table 3.

The sources, structural characterization and anti-pulmonary fibrosis activities of natural polysaccharides from fungi.

Name/source/ Structural characterization Experimental model Effects Reference
Cordyceps Mw: 2 × 105 Da In vivo: pingyangmycin-induced ICR mice. In vivo, cordyceps polysaccharide increased the IL-1RA levels, decreased the hydroxyproline content and shrank the fibrosis area in pingyangmycin-induced PF model mice. Hu et al. (2019)
FYGL-1/G. lucidum Mw: 7.8 × 104 Da; consisted of Gal, Rha and Glc in a mole ratio of 1.00: 1.15: 3.22; backbone structure: 1,2-linked β-l-Rhap, 1,3,6-linked α-d-Galp, 1,2,6-linked α-d-Glcp and 1-linked α- d-Glcp In vivo: BLM-induced adult male Sprague-Dawley rats. After FYGL-1 administration in BLM-induced PF model rats, the pulmonary index, inflammatory cell infiltration and collagen deposition reduced with upregulating the levels of glutathione, glutathione peroxidase, catalase, superoxide dismutase and downregulating the levels of malondialdehyde and hydroxyproline in the lung. Chen et al. (2016), Pan et al. (2012)
FMP-1/M. esculenta Mw: 4.7 × 103 Da; consisted of Man, Glc and Gal in a mole ratio of 1.00: 7.84: 1.24; backbone structure: →4)-α-d-Glcp-(1→,→6)-α- d-Galp-(1→ with α-1,6-d-Glcp, α-1,4-d-Glcp, β-1,6-d-Manpat a branching position of O-6. In vitro: H2O2-induced human alveolar epithelial cells (A549). In vitro, FMP-1 increased the cell viability with attenuating LDH release, decreased the cell apoptosis with attenuating the release of Cytochrome c and caspase-3, downregulated the expression levels of ROS and MDA, upregulated the activities of SOD and T-AOC in A549 cells, underlying antioxidative effect with PI3K/AKT/Nrf2/HO-1 signaling pathway. Cai et al. (2018), Li et al. (2018)
POL/O. lanpingensisa Mw: 3.2 × 105 Da; Containing Gal, Man and Glc in a ratio of 5.30: 13.38: 81.31 In vivo: BLM-induced male mice (C57BL/6). In vivo, POL improved histopathological changes, reduced collagen deposition and the accumulation of macrophages (inhibiting the expression levels of NOS2, CXCL10/IP10, MARCO and ST2), downregulated the expression levels of pro-inflammatory and pro-fibrogenic factors (TNF-α, IL-1β, IL-6, OSM,IL-10, IL-13, α-SMA, MCP-1 and TGF-β1) and inhibited MDA production with promoting SOD level in BLM-induced PF model mice. Zhou et al. (2020)