Pulmonary fibrosis (PF) emerges as a significant pulmonary sequelae in the convalescent phase of coronavirus disease 2019 (COVID-19), with current strategies neither specifically preventive nor therapeutic. Geum japonicum var. chinense (GJC) is used as a traditional Chinese medicine to effectively treat various respiratory conditions. However, the protective effects of GJC against PF remains unclear. In the present study, the anti-PF effect of GJC aqueous extract was studied using a PF mouse model induced by bleomycin (BLM). To characterize the metabolite changes related to PF and reveal therapeutic targets for GJC aqueous extract, we performed metabolomic and network analysis on mice lungs. Finally, key targets were then validated by Western blotting. GJC aqueous extract effectively alleviated the onset and progression of lung fibrosis in PF mice by inhibiting inflammatory responses and regulating oxidative stress levels. Integrating serum metabolomics and network analyses showed the arachidonic acid (AA) pathway to be the most important metabolic pathway of GJC aqueous extract against PF. Further validation of AA pathway protein levels showed a significant rise in the levels of ALOX5, PTGS2, CYP2C9, and PLA2G2A in PF lungs. GJC aqueous extract treatment regulated the above changes in metabolic programming. In conclusion, GJC is a promising botanical drug to delay the onset and progression of PF mice. The primary mechanism of action is associated with the comprehensive regulation of metabolites and protein expression related to the AA metabolic pathway.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and memory loss, for which effective pharmacological interventions remain limited. This study investigated the cognitive-enhancing effects of an optimized six‑herbal combination (HC) comprising Polygonati Rhizoma (PR), Lycium barbarum polysaccharides (LBPs), Green Tea (GT), Jujube Seeds (JS), Fructus hippophae (FH), and Mori Folium (MF). Using the Ellman method, we evaluated the acetylcholinesterase (AChE) inhibitory activities of individual herbs and HC. An L₂₅(4⁶) orthogonal design was employed to determine the optimal proportions of the six herbs, with AChE inhibition as the evaluation index. The optimal HC composition (PR 9 g, LBPs 6 g, GT 3 g, JS 3 g, FH 3 g, MF 5 g) exhibited 88.11% AChE inhibition at 2000 μg/mL, which was significantly higher than that of any individual herb (p < 0.05). Network pharmacology analysis revealed 682 common targets between HC and AD, with significant enrichment in the PI3K‑Akt signaling pathway, lipid metabolism, and chemical carcinogenesis‑receptor activation pathways, suggesting multi‑target mechanisms of action. In a D‑galactose‑induced subacute aging mouse model (3.5 g·kg⁻¹, 70 days), HC treatment (0.75, 1.5, and 3.0 g·kg⁻¹, 28 days) significantly improved spatial learning and memory in the Morris water maze. Specifically, HC at 1.5 g·kg⁻¹ significantly reduced escape latency (p < 0.01 vs. D‑galactose group), increased superoxide dismutase (SOD) and glutathione (GSH) levels (p < 0.05), and decreased malondialdehyde (MDA) and monoamine oxidase (MAO) levels (p < 0.01), while ameliorating hippocampal neuronal damage, as confirmed by hematoxylin and eosin staining. These findings demonstrate that HC exhibits potent anti‑cholinesterase activity, modulates oxidative stress, and protects against neuronal injury, positioning it as a promising multi‑target botanical candidate for further development in the prevention and management of AD.