Nitrate (NO₃⁻) and ammonium (NH₄⁺) are the main inorganic nitrogen (N) sources absorbed by oilseed rape, a plant that exhibits genotypic differences in N efficiency. In our previous study, the biomass, N accumulation, and root architecture of two oilseed rape cultivars, Xiangyou 15 (high N efficiency, denoted “15”) and 814 (low N efficiency, denoted “814”), were inhibited under NH₄⁺ nutrition, though both cultivars grew normally under NO₃⁻ nutrition. To gain insight into the underlying molecular mechanisms, transcriptomic changes were investigated in the roots of 15 and 814 plants subjected to nitrogen-free (control, CK), NO₃⁻ (NT), and NH₄⁺ (AT) treatments at the seedling stage. A total of 14,355 differentially expressed genes (DEGs) were identified. Among the enriched Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway categories of these DEGs, carbohydrate metabolism, lipid metabolism, protein metabolism, and cell wall biogenesis were inhibited by AT treatment. Interestingly, DEGs such as N transporters, genes involved in N assimilation and CESA genes related to cellulose synthase were also mostly downregulated in the AT treatment group. This downregulation of genes related to crucial metabolic pathways resulted in inhibition of oilseed rape growth after AT treatment.

Rheumatoid arthritis (RA) is a chronic disease that primarily manifests as symmetrical joint inflammation. Although Coix Seed Oil (CSO) has demonstrated anti-inflammatory effects in RA rat models, its systemic metabolic regulatory mechanisms remain unclear. Therefore, we aimed to investigate whether CSO ameliorates RA by modulating inflammation-associated metabolic pathways. Ultra-High-Performance Liquid Chromatography (UHPLC)-Q Exactive HF-X-MS-based metabolomics was used to profile metabolites in the synovial tissue and serum of complete Freund’s adjuvant (CFA)-induced RA rats. Systematically altered metabolites and their associated pathways were identified using multivariate analysis and pattern recognition. CSO treatment modulated 16 RA-related biomarkers in rat synovial tissues and 12 in the serum, which mainly affected amino acids, arachidonic acids, lipids, sphingolipids, and carnitines. These metabolites were associated with eight perturbed metabolic pathways that were predominantly involved in inflammatory responses. This study demonstrated that CSO has significant anti-RA effects on pharmacodynamic activity and metabolic network regulation. Additionally, inflammation-associated metabolic pathways are closely linked to the therapeutic efficacy of CSO in RA treatment.