Inflammatory bowel disease (IBD) is typically characterized by the dysregulation of Tfh cell differentiation. we sought to explore the potential mechanism of Ginsenoside Rg1 (G-Rg1) treated IBD by observing the level of the Tfh/Treg cells and the activation of PI3K/Akt signaling pathway in the colitis mice. In the present study, G-Rg1 significantly inhibited the inflammatory response to mice colitis induced by dextran sodium sulfate (DSS), as evidenced by increased body weight and colon length, decreased colon weight, reduced colon weight index and histopathological scores, lower levels of IL-6 and TNF-α, and increased IL-10 levels. Significantly, G-Rg1 effectively decreased the amounts of CD4+CXCR5+IL-9+(Tfh9), CD4+ CXCR5+IL-17+(Tfh17), and increased CD4+CXCR5+Foxp3+(Tfr) and CD4+CD25+ Foxp3+(Treg) cells. Furthermore, G-Rg1 markedly down-regulated PI3K and p-Akt level, and upregulated PTEN expression. These results indicated that G-Rg1 could effectively regulate the balance of Tfh/Treg cells to relieve experimental colitis, which could be potentially related to PI3K/Akt signaling pathway inhibition.
Keywords: Experimental colitis; Follicular helper T cells; Ginsenoside Rg1; P13K/Akt signal; Treg.
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