Qingjie Fuzheng granules treat ulcerative colitis by regulating Th17/Treg balance

Objective

To investigate the anti-inflammatory properties of Qingjie Fuzheng granules (QFG) in vivo using a dextran sulfate sodium (DSS)–induced ulcerative colitis (UC) model and elucidate the mechanism of which QFG alleviates UC by examining T cell 17 (Th17)/regulatory T cell (Treg) balance.

Methods

The DSS-induced UC murine model was established, and the mice were administered QFG or saline by gavage. Their general growth characteristics, including body weight, fecal occult blood, and disease activity index were observed, and the length of the colon was recorded. Hematoxylin and eosin staining was performed to examine pathological injury within the colon tissue. The expression levels of Th17-related cytokines, Treg-related cytokines, interferon-γ (IFN-γ), indoleamine 2,3-dioxygenase 1 (IDO1), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in the serum were detected by enzyme-linked immunosorbent assay or Bio-Plex immunoassay. Relative mRNA expressions in the spleen and colon tissues were detected by reverse transcription–quantitative polymerase chain reaction. The protein expressions of retinoic acid–associated orphan receptor γt (RORγt), Forked head/wing helix transcription factor 3 (Foxp3), or IDO1 were detected in the spleen and colon by western blotting or immunohistochemistry.

Results

QFG demonstrated the potential to improve the overall pathological conditions of DSS-induced UC mice as evidenced by significantly alleviating the colon shortening and improving colon tissue pathology. QFG also decreased expressions of the pro-inflammatory cytokines IL-1β, TNF-α, IFN-γ, and interleukin-6 as well as IDO1. QFG treatment significantly reduced the expressions of Th17-related cytokines and concurrently increased the expressions of Treg-related cytokines. After QFG treatment, the expression of transcription factor RORγt decreased in the colon and spleen, while that of the transcription factor Foxp3 increased.

Conclusion

QFG can suppress inflammation in mice with DSS-induced UC. This effect is achieved through the regulation of transcription factors RORγt and Foxp3, which inhibits Th17 ​cell differentiation, promotes Treg cell differentiation, and maintains Th17/Treg balance.