Background Network pharmacology is used with bioinformatic tools to broaden the understanding of drugs’ potential targets and the intersections with key genes of particular disease. Here we applied network pharmacology to collect testable hypotheses about the multi-targets mechanism of hydroxychloroquine (HCQ) against systemic lupus erythematosus (SLE). Methods Firstly, we predicted the potential targets of HCQ. Secondly, we got the related genes of SLE returned from databases. Thirdly, the intersections of the potential targets (HCQ) and related genes (SLE) were analyzed with gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. Finally, we validated our predictions of the potential targets by performing docking studies with HCQ. Results The results suggest that the efficacy of HCQ against SLE is mainly associated with the targets of cyclin-dependent kinase 2 (CDK2), estrogen receptor alpha (ESR1) and CDK1, which regulate PI3K/Akt/GSK3β as well as interferon (IFN) signaling pathway. Biological process of the network associated with the three targets is concentrated in the inhibition of immune response, negative regulation of gene expression and regulation of immune system process. Molecular docking analysis proves that hydrogen bonding and π-π stacking are the main forms of interaction. Conclusions Our research provides protein targets affected by HCQ in the treatment of SLE. Three key targets (CDK2, ESR1 and CDK1) involving 1766 proteins become the multi-targets mechanism of HCQ in the treatment of SLE. As well, the research also provides a new idea for introducing network pharmacology into the evaluation of the drugs with multi-targets in dermatology.

Melasma is an acquired, chronic, symmetrical hypermelanosis characterized by light to dark brown patches of hyperpigmentation on sun-exposed areas. To date, destruction of skin barrier, chronic inflammation and some other theories were thought to be related to the pathogenesis of melasma (Bellei & Picardo, 2020;Kang et al., 2011;Rodríguez-Arámbula et al., 2015). Previous research found that genes involved in the PPAR signaling pathway were down-regulated and genes involved the functions of stratum corneum barrier were up-regulated in melasma lesional skin (Chung et al., 2014). But there is a lack of evidence about the compositional analysis of the epidermal lipids related to the skin barrier of melasma.Skin surface lipid (SSL) is indispensable for epidermal barrier. It is a mixture of sebaceous gland lipids and intercellular lipids located in the outer layer of epidermal cells. SSL plays an important role in maintaining the skin barrier function and helps to regulate various aspects of the integumentary system, including skin barrier, cell proliferation, cell apoptosis, immunity, and inflammation . The lipids contained in SSL include ceramides(Cers), cholesterol, glycerophospholipids, free fatty acids, and glycerolipids.Lipid could influence skin status through several mechanisms, but there is a major limitation to identify lipid modifications because of the complexity of lipid composition (Jia et al., 2018). Such situation

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Network pharmacology is an emerging discipline that designs drugs based on systems biology theory and biological system network analysis. Here, we applied network pharmacology to analyze the multi-target mechanism of Cyclosporin A in the treatment of vitiligo First, we predicted the targets of Cyclosporin A. Second, we obtained the genes related to vitiligo from the database. Third, we constructed the PPI network of the mutual genes between Cyclosporin A and vitiligo and used gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) to analyze. Finally, we verified the prediction of potential targets through a docking study with Cyclosporin A. We found that there were 15 shared target genes between Cyclosporin A and vitiligo. We analyzed these 15 genes by Cytoscape and obtained a network diagram of 885 nodes.Through screening and molecular docking, PRKDC, CUL7, CUL1, HSPA8, HSPA4, and SIRT7 were the most likely multi-target mechanism of Cyclosporin A in the treatment of vitiligo. In our study, Cyclosporin A might not only affect the repair of DNA strands by targeting PRKDC, but also affected the innate and adaptive immune function of vitiligo patients by the targets of CUL1, CUL7, and HSP70. In addition, Cyclosporin A might promote the repigmentation of vitiligo by adjusting the expression of SIRT7.

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Background/objective: Recent studies have described an association between altered skin microbial community and epidemiology of skin diseases, such as vitiligo, atopic dermatitis and psoriasis. In this study, we conducted microbiological analysis on patients at different stages of vitiligo to determine whether the dysbiosis is associated with disease progression. Methods:To characterise the skin microbes in vitiligo patients, we profiled samples collected from 40 patients with active and stable vitiligo using the Novaseq sequencer. Alpha diversity was used to measure richness and uniformity, while Beta diversity (Non-Metric Multi-Dimensional Scaling) analysis was used to show the differences. Moreover, the species differences were evaluated by LEfSe analysis and the flora gene function was predicted using Statistical Analysis of Metagenomic Profiles (STAMP). Results:The alpha diversity results showed no significant differences between active vitiligo and stable vitiligo, while beta diversity and LEfSe analysis results showed the differences in community composition. Streptomyces and Streptococcus were enriched in active vitiligo compared to stable vitiligo. In addition, the flora gene function of mixed acid fermentation was more pronounced in active vitiligo, while the function of lipid IVA biosynthesis was more significant in stable vitiligo. Conclusion:This study has shown the differences in epidermal microbes between active vitiligo and stable vitiligo. Our results suggest that maintaining the flora balance might be a potential therapeutic target for vitiligo.

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