中文摘要：

目的：探讨DPP4抑制剂Sitagliptin对脂多糖（LPS）诱导胰岛β细胞炎症反应的影响及可能机制。方法 Sitagliptin与LPS同时或分别处理RINm细胞一定时间，采用RT-PCR法检测IL-6 mRNA水平，Western blot法检测细胞内IL-6水平及IκBα蛋白磷酸化水平。结果 RT-PCR结果显示，LPS＋Sitagliptin组与LPS组相比IL-6 mRNA水平明显下降（P＜0.01）。Western blot结果显示，LPS＋Sitagliptin组较LPS组IL-6蛋白水平稍有下降，但无统计学意义（P＞0.05）；LPS＋Sitagliptin组细胞内IκBα蛋白磷酸化水平较LPS组明显降低（P＜0.01）。结论 DPP4/CD26抑制剂在一定程度上能够抑制LPS诱导的IL-6 mRNA表达及IκBα蛋白磷酸化，其作用机制可能与DPP4/CD26抑制剂干扰NF-κB炎症通路有关。

英文摘要：

Objective To investigate the effect of DPP4/CD26 inhibitor on LPS-induced inflammation in isletβcells, and to explore the possible mechanism. Methods RINm cells were cultured with LPS alone or combined with sitagliptin in a time, using RT-PCR to detect the level of IL-6 mRNA, and the expression of IL-6 and the phosphorylation of IκBα protein were detected by western blot. Results The level of IL-6 mRNA in LPS＋Sitagliptin group obviously declined compared with LPS group （P〈0.01）; the expression of IL-6 protein in LPS＋Sitagliptin group slightly declined compared with LPS group, but with no statistical difference （P〉0.05）; the phosphorylation level of IκBα protein in LPS＋Sitagliptin group significantly decreased compared with LPS group （P〈0.01）. Conclusion DPP4/CD26 inhibitor can effectively inhibit the expression of IL-6 mRNA and the phosphorylation of IκBα protein which were induced by LPS. The mechanism may be related to DPP4/CD26 involved in LPS-activated NF-κB inflammatory pathway.