Baicalin, a
flavonoid, has a wide range of pharmacological properties, including
immunomodulation. The objective of this study was to investigate the effect of
baicalin on the balance of T helper 17 (Th17) and regulatory T (Treg) cells in a
colitis model. The rat
colitis model was induced by
2,4,6-trinitrobenzene sulfonic acid (TNBS).
Baicalin (10 ml/kg, each) or
mesalazine (positive control) was then administered orally for 7 days. Inflammatory and immunological responses were evaluated by pathology,
enzyme-linked
immunosorbent assay, real-time polymerase chain reaction, western blot analysis, and flow cytometry. Our study showed that
baicalin not only significantly attenuated TNBS-induced
colitis by reducing the disease activity index as well as macroscopic and microscopic scores, but it also improved the
weight loss and shortening of the colon.
Baicalin treatment also induced a significant decrease in the levels of inflammatory mediators, including the
myeloperoxidase activity, the levels of
tumor necrosis factor α, IL-1β, and Th1-related
cytokines IL-12 and IFN-γ. Furthermore, the beneficial effects of
baicalin seem to be associated with regulation of the Th17 and Treg paradigm. We found that administration of
baicalin significantly downregulated the number of Th17 cells and the levels of Th17-related
cytokines (IL-17 and IL-6) and
retinoic acid receptor-related orphan receptor γt. In contrast, there was an increase in Treg cells numbers, Treg-related
cytokines transforming growth factor-β and
IL-10, and forkhead box P3. Our results suggest that the anti-inflammatory effect of
baicalin may be linked to modulation of the balance between Th17 and Treg cells in TNBS-induced
ulcerative colitis.