Quercetin (QCT) is a bioflavonoid derived from vegetables and fruits that has anti-inflammatory and anti-ferroptosis effects against various diseases. Previous studies have shown that QCT modulates the production of cellular inflammatory factors in asthma models and delays the development of chronic airway inflammation. However, the regulatory mechanism of QCT, a traditional Chinese medicine, in the treatment of asthma has not been elucidated. The aim of the present study is to investigate whether QCT can inhibit ferroptosis via the SIRT1/Nrf2 pathway and play a therapeutic role in asthma. An ovalbumin-induced mouse asthma model was established, and its function was verified by hematoxylin eosin staining, enzyme linked immunosorbent assay, ferric ion assay, malondialdehyde and superoxide dismutase assays, dihydroethidium staining, immunohistochemical staining, western blotting, and quantitative real-time polymerase chain reaction. Our results indicated that an ovalbumin-induced asthma mouse model had been successfully established and that QCT inhibited inflammation, reduced serum levels of inflammatory factors IL-4, IL-5 and IL-13, increased superoxide dismutase levels in lung tissue homogenates, and reduced malondialdehyde and ferric ion production in asthmatic mice. In addition, we found that QCT was able to reverse the expression of SIRT1, Nrf2 and HO-1 in an in vivo asthma mouse model. The data from this study indicate that QCT can alleviate asthma, and its mechanism is related to the regulation of ferroptosis, oxidative stress, and the expression of SIRT1 protein.
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