Abstract
BackgroundAcne vulgaris is a common skin disease that affects the pilosebaceous unit, and inflammation plays an important role. Chinese traditional medicine Tanreqing (TRQ) has been used in the field of dermatology to treat inflammatory diseases and has shown outstanding efficacy. The purpose of this study was to evaluate the potential advantages of TRQ on a mouse model of acne inflammation. Additionally, network pharmacology and transcriptome analysis were utilized to investigate the possible underlying mechanisms. MethodsThe active compounds of TRQ were collected through TCMSP database and literature review, and the predicted targets of active compounds were obtained from Swiss Target Prediction. Acne targets were collected from the Gene Cards database and DisGeNET. Cytoscape v3.7.1 was used to build the "compounds-targets" network and PPI network and to obtain the core network. GO analysis and KEGG pathway annotation were performed on the core genes. The Illumina HiSeq sequencing platform was utilized to sequence mRNA from mouse skin tissue in acne areas. Differential gene expression analysis was conducted to identify genes that were affected by TRQ, and their associated biological functions and signaling pathways were analyzed. The transcriptomic and network pharmacology analyses were integrated to generate predictive results. Additionally, the efficacy of TRQ in treating acne was confirmed through H&E staining, and the predicted outcomes were verified through quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). ResultsThe study's results indicate that 37 potential target genes were enriched in multiple signaling pathways, including the atherosclerosis, IL-17, and TNF signaling pathways, according to network pharmacology. In addition, 338 transcriptomic DEGs were found to be involved in various signaling pathways, including Cell adhesion molecules and the IL-17 signaling pathway.The combined analysis of these findings suggests that the IL-17 and TNF signaling pathways are the primary mechanisms by which TRQ exerts its anti-acne effects. H&E staining revealed that TRQ inhibited inflammatory cell infiltration in acne lesions and attenuated the inflammatory response in acne. Moreover, TRQ significantly suppressed key factors such as TNF-α, JNK2, IL-17A, C/EBPβ, IL-6, and IL-1β in the IL-17 and TNF signaling pathways. Furthermore, TRQ also demonstrated a significant inhibition in the expression of TNF-α and IL-1β in the skin tissues of acne vulgaris mice ConclusionOur findings suggest that TRQ may effectively inhibit the IL-17/TNF signaling pathway by suppressing the expression of TNF-α and IL-1β, making it a potential candidate for the treatment of acne
Published Version
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