Eosinophilic asthma is the predominant phenotype of asthma, and although these patients are sensitive to glucocorticoid therapy, they also experience many side effects. Lonicerin is a kind of bioflavonoid isolated from the Chinese herb Lonicera japonica Thunb, which has anti-inflammatory and immunomodulatory effects. The aim of this study was to elucidate the effects of lonicerin on eosinophilic asthma and its potential mechanisms. Here, we established a house dust mite (house dust mite)-induced eosinophilic asthma model in BALB/c mouse, and evaluated the effects of lonicerin on it. Our results showed that lonicerin significantly reduced airway hyperresponsiveness the number of inflammatory cells (especially eosinophils) and the elevation of interleukin (IL)-4, IL-5, IL-13 and eotaxin in bronchoalveolar lavage fluid (BALF) supernatants of mice. Additionally, lonicerin also eminently blunted inflammatory infiltration and mucus secretion, as well as mRNA levels of Mucin 5AC (MUC5AC) in lung tissue. Furthermore, results of network pharmacology and molecular docking revealed that Src kinase and epidermal growth factor receptor may be the potential targets responsible for the effects of lonicerin. Finally, in vivo experiments confirmed that lonicerin inhibited activation of the Src/EGFR pathway by decreasing their phosphorylation. Taken together, the present study demonstrated that lonicerin could suppress HDM-induced eosinophilic asthma in mice through inhibiting the activation of Src/EGFR pathway, which also provides a basis for further research as a new potentially therapeutic agent for eosinophilic asthma and its underlying mechanisms in the future.

Non-small cell lung cancer (NSCLC) is a heterogeneous disease, which makes the prognostic prediction challenging. Cuproptosis, a recently discovered mode of regulated cell death (RCD), may be associated with the development of multiple diseases. However, the prognostic value of cuproptosis-related genes in NSCLC remains uncertain. In this study, we obtained the mRNA expression profiles and corresponding clinical data of NSCLC patients online and made some analysis. Our results showed that 16 cuproptosis-related genes were differentially expressed between NSCLC and normal tissues. GO and KEGG enrichment analysis revealed that these genes were mainly enriched in cellular energy metabolism-related pathways. According to the survival analysis of these 16 genes, the up-regulation of 13 genes predicted a poor overall survival (OS) rate in patients with NSCLC. Then, A 13-genes signature model was built to distinguish the patients into two risk groups. Patients in the high-risk group showed significantly a poor OS rate compared with patients in the low-risk group (P < 0.001 in the TCGA cohort). The tumor grade, tumor stage, and tumor vascular invasion also differ in two groups (P < 0.01 in the TCGA cohort). Receiver operating characteristic (ROC) curve analysis proved the model's predictive capacity. The same model was used in the ICGC cohort and similar results were confirmed. Finally, we verified the differential expression of several genes in our model between NSCLC and normal tissues. By detecting intracellular Cu2+ levels before and after gene knockdown, we found that four genes may affect the progression of NSCLC by regulating cuproptosis. In conclusion, a novel cuproptosis-related gene signature can predict the prognostic of NSCLC. Targeting cuproptosis may be a therapeutic approach for NSCLC.