The Th17/treg Regulation Of Triptolide On Trinitrobenzene Sulfonic Acid-induced Colitis In Mouse

Objective To investigate the regulation of triptolide on intestinal mucosa Th17/Treg balance on trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Methods Forty male BALB/C mice were randomly divided into 4 groups:control group, model group, low-dose and high-dose triptolide groups. Model group, low-dose and high-dose triptolide groups were induced colitis in mice by TNBS, low-dose and high-dose triptolide groups were intraperitoneally administrated in 35μg/kg or 70μg/kg triptolide every day, model group was intraperitoneally administrated in normal sodium every day, control group was given 50% alcohol enema and intraperitoneally administrated in normal sodium. All mices were sacrificed after two weeks, colonic tissue was evaluated by macroscopic and microscopic score in every group. The expression of IL17, RORC and Foxp3 mRNA in colonic tissues were assessed by real-time fluorescent quantitative reverse transcriptase polymerase chain reaction (RT-PCR).Results Low-dose and high-dose of triptolide group were significantly lower than model group on macroscopic and histological scores (P<0.05), the expression of IL17and RORC mRNA in colonic tissues was significantly lower than model group(0.16±0.02 vs 0.09±0.01 vs 1.04±0.14, P<0.05; 0.32±0.02 vs 0.22±0.04 vs 0.68±0.08, P<0.05), the expression of Foxp3 mRNA was significantly higher than model group(1.13±0.14 vs 1.16±0.20 vs 0.46±0.18, P<0.05), low-dose and high-dose of triptolide groups and control group weren't statistically significant(P>0.05).Conclusion Triptolide can inhibite Th17 cell differentiation and IL-17 generation through downregulation RORC, it can promote Treg cell development through upregulation Foxp3. Triptolide effectively inhibits inflammation in TNBS-induced colitis in mice through regulation Th17/Treg balance.