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Protonation, Fe2+ and solvent can induce different acidic structures and Lewis activity of Fe-IL by analyzing the slope of IA(X) ∼ n(Py).

The oxidation activity and solvation effect of iron-based ionic liquid (BmimFeCl4) are significantly affected by the structure and polarity of the added solvents.

Background Ferroptosis is a kind of regulated cell death, widely involved in lung diseases, including asthma. Macrophages are vital regulators in ferroptosis, and ferroptosis could promote M1 macrophage polarization. Quercetin (QCT), a kind of natural dietary flavonoid, could be an alternative treatment for ferroptosis and asthma. However, whether QCT could reduce ferroptosis in neutrophilic asthma (NA) remains to be described. Materials: A NA model was conducted to investigate the therapeutic function of QCT and ferrostatin-1 (Fer-1, ferroptosis inhibitor). Macrophage cell line, RAW 264.7 cell, was stimulated with LPS and QCT, Fer-1. The cell viability, inflammatory cytokines, were measured in all groups. The mitochondria morphological changes, malonaldehyde (MDA) levels and ferroptosis pathway proteins were also detected. Results In our study, QCT restored mitochondrial morphologic changes of lung tissues by reducing MDA level and increasing ferroptosis anti-oxidant markers proteins level (SLC7A11 and GPX4) in NA mouse model. In vitro experiment, QCT reduced macrophage ferroptosis, through upregulating cell viability and proteins level (SLC7A11 and GPX4), and reducing MDA level. Furthermore, we investigated that Fer-1 could inhibit M1 polarization, suggesting ferroptosis could promote M1 polarization. And QCT could inhibit M1 macrophage polarization in vitro and in vivo, just as Fer-1 did. Conclusion Our study first indicated that ferroptosis occurred in NA, and first demonstrated QCT could be a promising ferroptosis inhibitor in NA treatment. Besides, ferroptosis occurred in M1 macrophages phenotypes, and QCT could inhibit the M1 macrophage polarization, as Fer-1 did.