Published online Nov 7, 2014. doi: 10.3748/wjg.v20.i41.15299
Revised: June 8, 2014
Accepted: June 26, 2014
Published online: November 7, 2014
Processing time: 217 Days and 7.2 Hours
AIM: To evaluate the role of baicalin in ulcerative colitis (UC) with regard to the CD4+CD29+ T helper cell, its surface markers and serum inflammatory cytokines.
METHODS: Flow cytometry was used to detect the percentage of CD4+CD29+ cells in patients with UC. Real time polymerase chain reaction was used to detect expression of GATA-3, forkhead box P3, T-box expressed in T cells (T-bet), and retinoic acid-related orphan nuclear hormone receptor C (RORC). Western blotting was used to analyze expression of nuclear factor-κB (NF-κB) p65, phosphorylation of NF-κB (p-NF-κB) p65, STAT4, p-STAT4, STAT6 and p-STAT6. The concentrations of interferon-γ (IFN-γ), interleukin (IL)-4, IL-5, IL-6, IL-10 and TGF-β in serum were determined by ELISA assay.
RESULTS: The percentages of CD4+CD29+ T cells were lower in treatment with 40 and 20 μmol/L baicalin than in the treatment of no baicalin. Treatment with 40 or 20 μmol/L baicalin significantly upregulated expression of IL-4, TGF-β1 and IL-10, increased p-STAT6/STAT6 ratio, but downregulated expression of IFN-γ, IL-5, IL-6, RORC, Foxp3 and T-bet, and decreased ratios of T-bet/GATA-3, p-STAT4/STAT4 and p-NF-κB/NF-κB compared to the treatment of no baicalin.
CONCLUSION: The results indicate that baicalin regulates immune balance and relieves the ulcerative colitis-induced inflammation reaction by promoting proliferation of CD4+CD29+ cells and modulating immunosuppressive pathways.
Core tip: Ulcerative colitis is a kind of chronic and non-specific inflammatory bowel disease. Researchers believe that several distinguishing factors such as immune systems, genes and environment are likely necessary to result in ulcerative colitis (UC). The study here demonstrated that baicalin might be a potential immune inhibitor. It adjusted immune balance and relieved the inflammatory response caused by UC, probably by inhibiting the ratio of CD4+CD29+ cells and immunosuppressive pathways. Our results provide valuable information for further studies on the pathogenesis of UC and for the development of new drugs, and also provide a new view of studying T helper cell immune disorder-related diseases including UC.