Ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS/MS) was used to analyze the differences in chemical composition of dried and baked ginger.Then, network pharmacology was applied to investigate the mechanisms underlying their differences in efficacy. The chemical components of dried and baked ginger were analyzed using UPLC-Q-TOF-MS/MS, and the differential compounds were screened using partial least squares-discriminant analysisand random forest methods. SuperPRED and GeneCards databases were employed to retrieve drug and disease targets, respectively.Common targets were identified using Venn diagram mapping. Protein-protein interaction networks were constructed using the STRING database, and key targets were subjected to GO and KEGG enrichment analyses using the DAVID database.The UPLC-Q-TOF-MS/MS identified 61 chemical components, screening out 13 differential compounds (e.g., 7-gingerol, 12-gingerol, and gingerenone A). The network pharmacology results revealed that dried ginger mainly acts on targets such as MAPK1, PTGS1, and OPRD1, mediating the expression of signaling pathways such as interleukin-17, toll-like receptor, and TNF to alleviate inflammatory responses, exerting a “warming the middle to relieve pain” effect. Baked ginger mainly targets APEX1, SLC6A5, and NFKB1, mediating the HIF-1 signaling pathway, neurotrophin signaling pathways, and apoptosis to block pain signal transmission, exerting a “warming the middle to dispelling cold” effect. By integrating chemical composition analysis and network pharmacology, this study elucidated the mechanisms underlying the distinct therapeutic effects of dried and baked ginger, providing a scientific basis for their clinical applications.

We investigated the molecular mechanisms underlying the treatment of recurrent aphthous ulcers (RAU) using the Radix Aconiti-Cortex Phellodendri combination, based on weighted gene co-expression network analysis (WGCNA) and network pharmacology. A total of 301 active compounds were identified from the Radix Aconiti-Cortex Phellodendri combination, associated with 3 273 potential targets.WGCNA was used to analyze RAU-related genes. The Venn diagram package in R software was employed to identify intersections between drug-related targets and WGCNA modules. Pathway and process enrichment analyses, along with hierarchical clustering, were conducted using KEGG Pathway, GO Biological Processes, and Reactome Gene Sets. These analyses highlighted involvement in apoptosis regulation and signaling, glutathione metabolism, PI3K signaling abnormalities, resistance to epidermal growth factor receptor tyrosine kinase inhibitors, cytokine signaling in the immune system, the PPAR-α pathway, and other processes related to immune regulation, metabolism, and tissue repair.Using the MCODE plugin in Cytoscape v3.7.2, key hub genes within functional modules were identified, including ERBB2, CD44, NFKB1, and MMP2. Molecular docking showed that ERBB2 interacted with most active compounds; diterpenoid alkaloids from Aconitum and flavonoids from Phellodendron primarily targeted CD44; alkaloids from Phellodendron targeted MMP2; and both monoester and diester Aconitum alkaloids mainly targeted NFKB1. These findings suggest a complementary and synergistic effect between the two herbs in preventing RAU recurrence.Experimental validation showed that benzoylmesaconine, a core compound, significantly reduced LPS-induced ROS levels in macrophages, indicating thatRadix Aconiti, as the principal herb (Jun Yao), exerts its therapeutic effects primarily through metabolic regulation.

Betukladin is a dietary supplement composed of reindeer lichen powder and birch bark extract, possessing various pharmacological activities such as blood glucose regulation, lipid lowering, anti-inflammatory effects, and anticoagulation. This study investigates the lipid-lowering activity and underlying mechanism of Betukladin, aiming to validate its efficacy and provide a scientific basis for developing safe and economical natural lipid-lowering drugs. Using a zebrafish hyperlipidemia model, we found that Betukladin significantly improved the elevated Oil Red O staining integrated optical density values, triglyceride levels, and total cholesterol levels induced by high-fat modeling, indicating its lipid-lowering activity. Network pharmacology analysis suggested that Betukladin may exert its lipid-lowering effects through multiple coordinated pathways, including lipid and atherosclerosis pathways and the PPAR signaling pathway. RT-qPCR results showed that it can regulate lipid metabolism-related genes (apoA1, LDLR, and ANGPTL3), fatty acid synthesis and oxidation genes (SREBF1, FASN, PPARα, and cpt1a,), and cholesterol metabolism-related genes (CYP7A1, HMGCR, ABCG5, and ABCG8).