<p class="first" id="d3233148e140">Acute lung injury (ALI) is a common lung disease
accompanied by acute and persistent
pulmonary inflammatory response syndrome, which leads to alveolar epithelial cells
and capillary endothelial cell damage. Yam glycoprotein, separated from traditional
Chinese yam, has been shown to have anti-inflammatory and immunomodulatory effects.
In this experiment, we mainly studied the therapeutic effect and mechanism of a glycoprotein
on the lipopolysaccharide (LPS)-induced ALI mice. An oral glycoprotein method was
used to treat the mouse ALI model induced by LPS injection in the peritoneal cavity.
Afterward, we measured the wet/dry (W/D) ratio, the activity of myeloperoxidase (MPO),
the oxidative index superoxide dismutase (SOD), malondialdehyde (MDA), glutathione
peroxidase (GSH-PX) and the production of inflammatory cytokines interleukin-1β (IL-1β),
tumour necrosis factor-α (TNF-α), and interleukin-6 (IL-6) to evaluate the effect
of yam glycoprotein on lung tissue changes. We examined the protein expression of
TLR4, ASC, NF-κBp65, p-NF-κBp65, Caspase-1, IκB, NLRP3, p-IκB, and β-actin by western
blot analysis. Immunohistochemical analyses of NLRP3 and p-p65 in lung tissue were
carried out to assess the mechanism of glycoprotein action. This result suggests that
glycoprotein markedly depressed LPS-induced lung W/D ratio, MPO activity, MDA content
SOD and GSH-Px depletion, and the contents of inflammatory cytokines IL-1β, IL-6,
and TNF-α. Moreover, glycoprotein blocked TLR4/NF-κBp65 signaling activation and NLRP3inflammasome
expression in LPS-induced ALI mice. As this particular study shows, glycoprotein has
a safeguarding effects on LPS-induced ALI mice, possibly via activating NLRP3inflammasome
and TLR4/NF-κB signaling pathways.
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