As a classic prescription, Huangqin Tang (HQT) has been widely applied to treat ulcerative colitis (UC), although its pharmacological mechanisms are not clear. In this study, urine metabolomics was first analysed to explore the therapeutic mechanisms of HQT in UC rats induced by TNBS. We identified 28 potential biomarkers affected by HQT that might cause changes in urine metabolism in UC rats, mapped the network of metabolic pathways, and revealed how HQT affects metabolism of UC rats. The results showed that UC affects amino acid metabolism and biosynthesis of unsaturated fatty acids and impairs the tricarboxylic acid cycle (TCA cycle). UC induced inflammatory and gastrointestinal reactions by inhibiting the transport of fatty acids and disrupting amino acid metabolism. HQT plays key roles via regulating the level of biomarkers in the metabolism of amino acids, lipids, and so on, normalizing metabolic disorders. In addition, histopathology and other bioinformatics analysis further confirm that HQT altered UC rat physiology and pathology, ultimately affecting metabolic function of UC rats.

In this study, we explored the pharmacological mechanisms of Huangqin Tang (HQT; a traditional Chinese medicine formula) in ulcerative colitis (UC) and provided evidence for potential roles HQT plays by gene expression profiling. The UC rat model was made via a compound method (trinitrobenzene sulfonic acid plus ethanol). After a ten-day treatment, microarray analysis was performed from the colon segment of the rats. Biological functions and specific signaling pathways were enriched based on differentially expressed genes (DEG), and corresponding gene networks were constructed via Ingenuity Pathway Analysis (IPA). Through the network, we screened the potential "candidate targets," such as ITGB1, FN1, CASP3, and ITGA5 and FABP1, ABCB1, FABP2, and SLC51B. These potential candidate targets were functionally related to immune responses, inflammation, and metabolism. Moreover, HQT significantly decreased serum levels of proinflammatory factors nitrogen monoxide (NO), proinflammatory cytokines interleukin- (IL-) 17, and prostaglandin E2 (PGE2). The degree of HE staining of colonic tissue was severe in the model group but reduced significantly in the HQT group. HQT exhibited protective effects against colon damage by inhibiting the inflammatory response.

Influenza A virus (IAV) infection triggers excessive activation of PANoptosis—a coordinated form of programmed cell death integrating pyroptosis, apoptosis, and necroptosis—which contributes to severe immunopathology and acute lung injury. However, the molecular regulators that drive PANoptosis during IAV infection remain poorly understood. In this study, we integrated bulk and single-cell RNA sequencing (scRNA-seq) datasets to dissect the cellular heterogeneity and transcriptional dynamics of PANoptosis in the influenza-infected lung. PANoptosis-related gene activity was quantified using the AUCell, ssGSEA, and AddModuleScore algorithms. Machine learning approaches, including Support Vector Machine (SVM), Random Forest (RF), and Least Absolute Shrinkage and Selection Operator (LASSO) regression, were employed to identify key regulatory genes. scRNA-seq analysis revealed that PANoptosis activity was primarily enriched in macrophages and neutrophils. Integration of transcriptomic and computational data identified cathepsin B (CTSB) as a central regulator of PANoptosis. In vivo validation in an IAV-infected mouse model confirmed elevated expression of PANoptosis markers and upregulation of CTSB. Mechanistically, CTSB may facilitate NLRP3 inflammasome activation and promote lysosomal dysfunction-associated inflammatory cell death. These findings identify CTSB as a critical mediatoCTSBr linking lysosomal integrity to innate immune-driven lung injury and suggest that targeting CTSB could represent a promising therapeutic strategy to alleviate influenza-associated immunopathology.

Angelicin (Ang), a natural tricyclic aromatic compound and quality marker derived from Fructus Psoraleae, exhibits significant anti-inflammatory efficacy. Fructus Psoraleae has long been utilized clinically for treating ulcerative colitis (UC). However, the specific role of Ang in UC remains poorly characterized. The present study aimed to elucidate the anti-UC effects of Ang and its underlying mechanisms. The anti-UC activity of Ang was evaluated using two UC models induced by dextran sulfate sodium (DSS) and 2,4,6-trinitrobenzenesulfonic acid (TNBS). Results demonstrated that Ang markedly inhibited the progression of UC. Microbial profiling indicated that the Ang-treated microbiome, particularly Lactobacillus murinus, provided protective effects against UC. Mechanistically, Ang facilitated proliferation of normal colonic epithelial cells, thus enhancing the intestinal mucosal barrier (IMB). Cysteine (Cys) played a crucial intermediary role by promoting glutathione (GSH) synthesis, maintaining redox homeostasis, and consequently facilitating cell proliferation. Additionally, increased Cys levels supported ribosomal biogenesis, enhancing protein translation and further stimulating cell proliferation. G-rich RNA sequence-binding factor 1 (GRSF1) was identified as a direct molecular target of Ang during ribosomal biogenesis. These findings indicated that Ang is a promising agent for promoting Cys-mediated cell proliferation, highlighting its role in maintaining redox homeostasis and protein translation. This study provides evidence supporting the future development of Ang as a therapeutic candidate for UC.