CAJ | 학술논문

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。
목적：탐토DPP4억제제Sitagliptin대지다당（LPS）유도이도β세포염증반응적영향급가능궤제。방법 Sitagliptin여LPS동시혹분별처리RINm세포일정시간，채용RT-PCR법검측IL-6 mRNA수평，Western blot법검측세포내IL-6수평급IκBα단백린산화수평。결과 RT-PCR결과현시，LPS＋Sitagliptin조여LPS조상비IL-6 mRNA수평명현하강（P＜0.01）。Western blot결과현시，LPS＋Sitagliptin조교LPS조IL-6단백수평초유하강，단무통계학의의（P＞0.05）；LPS＋Sitagliptin조세포내IκBα단백린산화수평교LPS조명현강저（P＜0.01）。결론 DPP4/CD26억제제재일정정도상능구억제LPS유도적IL-6 mRNA표체급IκBα단백린산화，기작용궤제가능여DPP4/CD26억제제간우NF-κB염증통로유관。
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.