Influence of glucosidorum tripterygii tororum on expression of interleukin-23, interleukin-17 and interleukin-12 in colonic tissues of mice with colitis / 第二军医大学学报

ABSTRACT

Objective: To study the influence of glucosidorum tripterygii tororum (GTT) and Mesalazine on the expression of IL-23, IL-17 and IL-12 in the colonic tissues of mice with rinitrobenzene sulphonic acid (TNBS)-induced acute colitis, and to study the possible mechanism. Methods: The C57BL/6 mice were divided into 4 groups, namely, a control group, a model group, a Mesalazine group and a GTT group. Colitis was induced by TNBS in the last 3 groups. The mice in the model group received no additional treatment; those in the GTT group received GTT daily by oral gavage 4 days before exposure to TNBS till the end of the experiment, and those in the Mesalazine group received Mesalazine enema solution daily 4 days before exposure till the end of the experiment. All the mice were sacrificed at 48 h after enema with TNBS. The macroscopic and histological scores of colon damage and myeloperoxidase (MPO) activity in colonic tissue were evaluated in every group. IL-23p19 and IL-17 contents in colonic tissues were measured by ELISA; the expression of IL-23p19, IL-17 and IL-12p35 mRNA in colonic tissues were examined by real-time fluorescent quantitative reverse transcriptase polymerase chain reaction (RT-FQ-PCR) with SYBR Green I. Results: Compared with the model group, GTT group and Mesalazine group had significantly lower macroscopic and histological scores and MPO activity (P<0.05). Expression of IL-23p19, IL-17 and IL-12p35 mRNA in the colonic tissues of the model group was significantly higher than that of the other 3 groups(P<0. 05); the expression of IL-23p19, IL-17 protein was significant higher in the model group than that in the other 3 groups (P<0. 05), with no significant difference found between the later 3 groups. Conclusion: GTT, like Mesalazine, can effectively inhibit inflammation in mice with TNBS-induced acute colitis through non-selectively inhibiting the expression of IL-23p19, IL-17 and IL-12p35.