DPP-4 (CD26) inhibitor sitagliptin exerts anti-inflammatory effects on rat insulinoma (RINm) cells via suppressing NF-κB activation
DPP-4 (CD26) inhibitor sitagliptin exerts anti-inflammatory effects on rat insulinoma (RINm) cells via suppressing NF-κB activation
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DOI：
10.1007/s12020-016-1073-8
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发表时间：
2017-03-01
期刊：
影响因子：
3.7
通讯作者：
Li, Yan
中科院分区：
文献类型：
--
作者：
Hu, Xingyun;Liu, Shanying;Li, Yan
二肽基肽酶-4 （CD26）是一种细胞表面糖蛋白，可在多种细胞中表达。二肽基肽酶-4 （CD26）参与了T细胞的活化。尽管如此，其在胰岛β细胞炎症作用中的作用尚未得到很好的研究。本研究利用经典的二肽基肽酶-4 （CD26）抑制剂西格列汀，研究二肽基肽酶-4 （CD26）对大鼠胰岛素瘤细胞nf - κ B活化、炎症因子表达及细胞凋亡的影响。结果表明，二肽基肽酶-4 （CD26）在大鼠胰岛素瘤细胞表面表达。西格列汀可抑制脂多糖诱导的大鼠胰岛素瘤细胞nf - κ B的激活和炎症因子的表达。此外，西格列汀治疗可减少脂多糖刺激的细胞凋亡。综上所述，本研究首次发现西格列汀抑制大鼠胰岛素瘤细胞NF-kappa B活化和炎症因子表达，提示二肽基肽酶-4抑制剂可能对胰岛β细胞具有直接的抗炎作用。
Dipeptidyl peptidase-4 (CD26), a cell surface glycoprotein, is expressed by a variety of cells. It has been shown that dipeptidyl peptidase-4 (CD26) is involved in T cell activation. Nonetheless, its role in inflammatory effects in islet beta cells has not been well investigated. In this study, we used sitagliptin, a classic inhibitor of dipeptidyl peptidase-4 (CD26), to research the effect of dipeptidyl peptidase-4 (CD26) on the activation of NF-kappa B, the expression of inflammatory cytokines, and cell apoptosis in rat insulinoma cells. Results showed that dipeptidyl peptidase-4 (CD26) was expressed on the surface of rat insulinoma cells. Lipopolysaccharide-induced NF-kappa B activation and expression of inflammatory cytokines were suppressed by sitagliptin treatment in rat insulinoma cells. Furthermore, sitagliptin treatment reduced cell apoptosis stimulated by lipopolysaccharide. Taken together, this study showed for the first time that sitagliptin suppressed NF-kappa B activation and inflammatory cytokines expression in rat insulinoma cells, suggesting that the dipeptidyl peptidase-4 inhibitor may exert direct anti-inflammatory effects in islet beta cells.