ArticleJournal of thoracic disease2026
Glycyrrhizin alleviates
Article in Journal of thoracic disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Methods: Forty specific pathogen-free male BALB/c (Bagg albino substrain c) mice (4-5 weeks old, 20±2 g) were randomly assigned to five experimental groups (n=8 per group): control, MP-low, MP-high, MP-high + ferrostatin-1 (Fer-1, a specific ferroptosis inhibitor), and MP-high + glycyrrhizin. The MP infection model was established via intranasal instillation for three consecutive days. On day 7 post-instillation, lung histopathology, bronchoalveolar lavage fluid (BALF) inflammatory profiles, pro-inflammatory cytokines [interleukin (IL)-6, tumor necrosis factor-α (TNF-α), IL-1β, interferon-gamma (IFN-γ)], oxidative stress markers [malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), reduced glutathione to oxidized glutathione (GSH/GSSG) ratio], tissue iron content, and ferroptosis-regulatory proteins (GPX4, ACSL4, HMGB1) were systematically evaluated. Results: The MP-low group induced only mild pulmonary changes with no statistically significant alterations in inflammatory or ferroptotic biomarkers compared to the control group (P>0.05). Conversely, the MP-high group caused severe ALI, characterized by markedly elevated BALF inflammatory cell infiltration and cytokine secretion (2.3- to 3.8-fold), increased tissue concentrations of MDA, 4-HNE, and ferrous iron (Fe Conclusions: Ferroptosis serves as a substantial pathological driver of MP-induced ALI. Glycyrrhizin effectively mitigates severe lung injury by inhibiting pulmonary ferroptosis through the modulation of the GPX4/ACSL4 axis and by suppressing secondary inflammatory cascades. These findings provide a novel mechanistic insight and an experimental therapeutic rationale for treating severe MP-associated respiratory complications in pediatric clinical settings.
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