Astilbin alleviates inflammatory response and mitigates psoriasis-like symptoms by modulating T helper 17/regulatory T cell differentiation balance through intestinal microbiota

Background: To explore the mechanism by which Astilbin ameliorates psoriasis-like symptoms through gut microbiota. Objectives: An imiquimod (IMQ)-induced psoriasis-like mouse model was established. Skin lesions were evaluated by Psoriasis Area and Severity Index, Hematoxylin and Eosin staining, and immunohistochemistry. Inflammatory cytokines (interleukin [IL]-17A, IL-22, and IL-23) were measured by Enzyme-Linked Immunosorbent Assay. Methods: The role of intestinal microbiota in Astilbin’s mitigation of psoriasis-like lesions was verified through fecal microbiota transplantation experiments. Flow cytometry was employed to determine the proportion of T helper 17 (Th17) and regulatory T cell (Treg), and quantitative reverse transcription polymerase chain reaction (qRT-PCR) was employed to test the expression of Retinoic acid receptor-related orphan receptor gamma t and Forkhead box protein P3. 16S rRNA sequencing was used to analyze fecal microbiota changes. Results: Results showed Astilbin reduced psoriasis-like skin damage, Ki67 expression, and cytokine secretion, suggesting that these effects are potentially dependent on gut microbiota. Astilbin decreased the Th17/Treg ratio, alleviating inflammation. Further 16S rRNA sequencing analysis indicated that Astilbin alleviated psoriasis in mice, possibly by reducing the abundance of Firmicutes and the proportion of Lachnospiraceae within Firmicutes . Thus, our data suggest that Astilbin may modulate Th17/Treg differentiation balance via gut microbiota to mitigate IMQ-induced psoriasis-like dermatitis in mice. Conclusion: Overall, our study supports that Astilbin alleviates inflammatory response, potentially by modulating Th17/Treg differentiation balance through intestinal microbiota, thereby reducing the severity of IMQ-induced psoriasis-like lesions in mice.