Identification of IL-17 as a Key Target Regulated by Allicin through RNA-seq
To further uncover the molecular mechanism of underlying disruption of IMQ-induced psoriasis development by allicin, we used RNA-sequencing (RNA-seq) to compare gene alternations between IMQ-treated and allicin-treated groups. A Volcano plot depicting changes in differentially expressed genes (DEGs) after Allicin treatment is shown in Figure 5A. Compared with the IMQ-treated group, 1285 genes were significantly altered, including 344 downregulated and 941 upregulated genes in the allicin-treated group (fold change≥2 and q<0.05). Among these DEGs, the downregulated genes were closely associated with inflammation (Figure 5B). KEGG analysis showed that the DEGs were involved in various signaling pathways, including cytokine−cytokine receptor interaction, basal cell carcinoma, Wnt signaling pathway, and IL-17 signaling pathway (Figure 5C). The gene expression level of IL-17A and IL-17F was significantly different, which further confirmed that allicin could alleviate IMQ-induced psoriasis-like skin inflammation in mice through the IL-17-mediated signaling pathway. GO enrichment analysis indicated that the downregulated DEGs were mainly enriched in biological processes associated with signal transduction and innate immune response (Figure 5D). Taken together, these results indicated IL-17-associated inflammatory genes and IL-17 signal pathways were regulatory targets of allicin in IMQ-induced psoriasis-like inflammatory skin.