雷公藤多苷对结肠炎小鼠结肠组织IL-23、IL-17和IL-12表达的影响

Influence of glucosidorum tripterygii tororum on expression of interleukin-23,interleukin-17 and interleukin-12 in colonic tissues of mice with colitis

目的:观察雷公藤多苷(GTT)、美沙拉嗪对三硝基苯磺酸(TNBS)诱导的急性结肠炎小鼠结肠组织中IL-23、IL-17、IL-12表达的影响,探讨其可能的作用机制。方法:C57BL/6小鼠随机分为4组:正常对照组、模型组、美沙拉嗪组、雷公藤多苷组,后3组应用TNBS建立小鼠急性结肠炎模型,模型组不作其他处理,雷公藤多苷组和美沙拉嗪组于造模前4d开始每天给予雷公藤多苷灌胃或美沙拉嗪灌肠液灌肠直到实验结束,正常对照组不作任何特殊处理。各组小鼠均于TNBS灌肠后48h处死,检测各组小鼠结肠组织大体、组织学损伤评分及髓过氧化物酶(MPO)活性;ELISA法检测结肠组织IL-23p19、IL-17蛋白含量,实时荧光定量RT-PCR检测结肠组织IL-23p19、IL-17、IL-12p35的mRNA表达。结果:美沙拉嗪组和雷公藤多苷组小鼠结肠大体及组织学损伤记分、MPO活性明显低于模型组(P<0.05);模型组结肠组织IL-23p19、IL-17、IL-12p35mRNA表达水平明显高于正常对照组、美沙拉嗪组、雷公藤多苷组(P<0.05);模型组结肠组织IL-23p19、IL-17蛋白水平明显高于正常对照组、美沙拉嗪组、雷公藤多苷组(P<0.05),后三者间无统计学差异。结论:雷公藤多苷可能通过非选择性抑制IL-23p19、IL-17、IL-12p35的表达来抑制结肠炎小鼠的炎症反应,效果与美沙拉嗪类似。

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 EIASA; 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.