Zuojinwan (ZJW), a classic herbal formula, has been extensively used to treat gastric symptoms in clinical practice in China for centuries. However, the pharmacological mechanisms of ZJW still remain vague to date. In the present work, a network pharmacology-based strategy was proposed to elucidate its underlying multi-component, multi-target, and multi-pathway mode of action against gastritis. First we collected putative targets of ZJW based on TCMSP and STITCH databases, and a network containing the interactions between the putative targets of ZJW and known therapeutic targets of gastritis was built. Then four topological parameters, “degree”, “betweenness”, “closeness”, and “coreness” were calculated to identify the major targets in the network. Furthermore, the major hubs were imported to the Metacore database to perform a pathway enrichment analysis. A total of 118 nodes including 59 putative targets of ZJW were picked out as major hubs in terms of their topological importance. The results of pathway enrichment analysis indicated that putative targets of ZJW mostly participated in various pathways associated with anti-inflammation response, growth and development promotion and G-protein-coupled receptor signaling. More importantly, five putative targets of ZJW (EGFR, IL-6, IL-1β, TNF-α and MCP-1) and two known therapeutic targets of gastritis (CCKBR and IL-12β) and a link target NF-κB were recognized as active factors involved in the main biological functions of treatment, implying the underlying mechanisms of ZJW acting on gastritis. ZJW could alleviate gastritis through the molecular mechanisms predicted by network pharmacology, and this research demonstrates that the network pharmacology approach can be an effective tool to reveal the mechanisms of traditional Chinese medicine (TCM) from a holistic perspective.

Lianling Tang (LLT), a traditional Chinese herbal decoction, is utilized for managing inflammatory skin conditions in China. This study explores the therapeutic effects and molecular mechanisms of LLT on atopic dermatitis (AD) in a mouse model, employing proteomics techniques. We evaluated the therapeutic efficacy of LLT on AD in mice by assessing skin inflammation scores, conducting histopathological examinations, and measuring serum levels of IgE, IL-4, and IL-6. Using Tandem Mass Tag (TMT) technology, we performed proteomics analysis of skin samples from Control, Model, LLT-treated, and positive control drug-treated mice, and identified differentially expressed proteins (DEPs). These proteins were then analyzed via GO and KEGG pathways to elucidate LLT's mechanisms in treating AD. LLT markedly reduced skin inflammation scores, epidermal thickening, and mast cell infiltration, and decreased serum IgE, IL-4, and IL-6 levels in AD model mice, highlighting its therapeutic potential. Proteomics analysis identified Staphylococcus aureus infection as a pivotal AD pathogenesis mechanism and revealed critical proteins such as C1QA, C4B, C5, and FCGR3. LLT's mechanisms, such as modulating the complement activation, and influencing phagocytosis, effectively reduce inflammation and alleviate symptoms caused by Staphylococcus aureus in AD. LLT shows potential in AD treatment by modulating pathways associated with Staphylococcus aureus infection, effectively alleviating symptoms.