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.