中文摘要：

目的探讨雷公藤甲素对三硝基苯磺酸（TNBS）诱导的结肠炎小鼠肠道Th17／Treg平衡的调节作用。方法40只BALB／c小鼠随机分为4组：对照组、模型组、雷公藤甲素低剂量组和高剂量组。模型组、雷公藤甲素低剂量组和高剂量组用TNBS诱导小鼠结肠炎模型，造模后，雷公藤甲素低剂量组和高剂量组分别腹腔注射35肛g·kg^-1·d^-1、70μg·kg^-1·d。雷公藤甲素，模型组每天腹腔注射生理盐水。对照组用50％乙醇溶液灌肠后每天腹腔注射生理盐水。2周后处死各组小鼠，评估各组小鼠结肠组织的大体和组织学评分，实时荧光定量RT-PCR检测结肠组织IL-17、RORC和Foxp3mRNA表达水平。结果雷公藤甲素低剂量和高剂量组小鼠结肠组织大体和组织学评分显著低于模型组（P〈0．05），结肠组织IL-17、RORCmRNA表达显著低于模型组（P〈0．05），Foxp3mRNA表达显著高于模型组（P〈0．05），雷公藤甲素低剂量、高剂量组与对照组比较，差异无统计学意义（P〉0．05）。结论雷公藤甲素可能通过下调RORC表达抑制Th17细胞分化、IL-17产生，上调Foxp3促进Treg细胞形成，从而调节结肠炎小鼠Th17／Treg平衡，抑制肠道炎症。

英文摘要：

Objective To investigate the regulation of triptolide on intestinal mucosa Thl7/Treg balance in trinitro- benzene sulfonic acid （TNBS）-induced colitis in mice. Methods Forty BALB/C mice were randomly divided into 4 groups： control group, model group, low-dose and high-dose of triptolide treated groups. Model group, low-dose andhigh-dose of triptolide groups were induced colitis in mice by TNBS; low-dose and high-dose triptolide groups were intra- peritoneally administrated in 35 μg/kg or 70 μg/kg triptolide every day ; model group was intraperitoneally administrated in normal saline. Control group was given 50% alcohol enema and intraperitoneally administrated in normal saline at the same time. All mice were sacrificed after two weeks, colonic tissue was evaluated by macroscopic and histological scorein every group. Expression of IL-17, RORC and Foxp3 mRNA in colonic tissues were assessed by real-time fluorescent quantitative reverse transcriptase polymerase chain reaction （ RT-PCR）. Results Macroscopic and histological scores in low-dose and high-dose of triptolide group were significantly lower than those in model group （ P 〈 0.05 ） , the expression of IL-17and RORC mRNA in colonic tissues were significantly lower than those in model group （P 〈 0.05） , and the ex- pression of Foxp3 mRNA was significantly higher than those in model group （P 〈 0.05）. There was no difference in low-dose and high-dose triptolide groups and control group （P 〉 0.05）. Conclusion Triptolide can inhibit Thl7 cell differentiation and IL-17 generation through downregulation RORC. It can promote Treg cell expression through upregu- lation Foxp3. Triptolide can effectively innhibit inflammation in TNBS-induced colitis in mice through regulation Thl7/ Treg balance.