Shaoying Yuan,Yan Zhang,Yixing Wu,Bing Liu,Wenkai Nie,Zhiming Ye,Huiwen Yang,Tianhui You
This study explores the mechanisms and potential targets of paeoniflorin (Pae) in treating atopic dermatitis (AD) through network pharmacology, molecular docking, and experimental validation. Pae, an active ingredient from Paeonia lactiflora Pall., exhibits immunomodulatory and anti-inflammatory effects. Literature from PubMed identified Pae, and its potential targets were predicted using tools like Swiss Target Prediction, Target Net, Super-PRED and Pharm Mapper databases. AD-related targets were obtained from DisGeNET and Gene Cards, and their intersection was analyzed using Venny. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses identified key pathways. Molecular docking confirmed Pae’s interaction with core targets. In vivo, AD was induced in mice using calcipotriol (MC903), and Pae's effects were assessed through dermatitis score, epidermal thickness, spleen index, and histopathology. In vitro, TNF-α-induced Human immortalized keratinocyte (HaCaT) cells were used to assess inflammation and apoptosis. Enzyme-linked immunosorbent assay (ELISA) and western blot (WB) analyzed inflammatory markers, while Hoechst staining measured apoptosis. Network pharmacology identified 229 predicted targets for the ingredient Pae, and 1,458 disease-associated targets for AD, finally revealed 63 common genes between them. Protein-Protein Interaction (PPI) analysis revealed 17 core targets. Experimental results showed Pae reduced dermatitis scores, epidermal thickness, spleen index, and inflammatory factors (IL-1β, IL-6, IgE, TNF-α, IL-8). Hoechst staining showed reduced apoptosis, and WB analysis revealed Pae's effects on MAPK and Apoptosis signaling pathways. These findings suggest Pae’s potential for AD treatment.
Rong Huang,Wenyu Zhang,Yueqi Hu,Junjie Xu,Zhihui Dong,Jikai Liu,Li Zhou
Atopic dermatitis (AD), a prevalent inflammatory skin condition, significantly impacts patients' quality of life due to the multifaceted etiology and the lack of targeted therapeutic options. As the “Chinese herbal antibiotic”, Houttuynia cordata is renowned for its diverse pharmacological attributes. This study aims to investigate the therapeutic potential of Houttuynia cordata polysaccharides (HCP) in treating AD and to elucidate the mechanisms involved. HCP alleviated AD in MC903-induced mice by reducing epidermal thickness, skin lesions, mast cell infiltration, inflammatory cytokines, and restoring barrier proteins. It also suppressed inflammatory cytokines/chemokines via the mitogen-activated protein kinase (MAPK) pathway in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and tumor necrosis factor-alpha (TNF-α)/ interferon-γ(IFN-γ)-induced human keratinocytes cells (HaCaT). Moreover, HCP modulated inflammation-related metabolic pathways, especially restored lipid metabolic homeostasis through upregulating phosphatidylcholine (PC) and downregulating triglyceride (TG), lysophosphatidylcholine (LPC), potentially alleviating AD-like lesions and restoring barrier function. Our findings underscore the promising potential of HCP as a topical therapeutic candidate for AD treatment, offering a new direction for the development of targeted AD therapies.
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