We attempt to explore the role of miR-217 during the process of type 2 diabetes mellitus (T2DM). Mouse β-TC-tet was dealt with 16.7 mM glucose (HG) to imitate the cells in T2DM. Cell proliferation and apoptosis were determined by cell counting kit-8 and flow cytometry. The correlation between miR-217 and Mafb was predicted with biological software and confirmed by dual lucifierase assay. Western blot was applied to detect protein expression. The data from GEO database exhibited that miR-217 was upregulated in T2DM patients. HG treatment upregulated the expression of miR-217, inhibited the proliferation, and promoted the apoptosis and inflammation of β-TC-tet cell. Depletion of miR-217 alleviated the damage of β-TC-tet cell caused by HG. Mafb was affirmed as a target of miR-217 and was negatively modulated by miR-217. Knockdown of Mafb attenuated the alleviation of miR-217 inhibitor on β-TC-tet cell damage. The expression of key proteins in NF-κB signaling pathway was upregulated by HG, and this upregulation tendency was inhibited by miR-217 inhibitor. Moreover, silencing Mafb could alleviate the inhibition of miR-217 inhibitor on these proteins. Our findings insinuated that inhibition of miR-217 could relieve β-TC-tet damage induced by HG through regulating Mafb and NF-κB signaling.

我们试图探索miR-217在2型糖尿病（T2DM）过程中的作用。用16.7 mM葡萄糖（HG）处理小鼠β-TC-tet，以模仿T2DM中的细胞。通过细胞计数试剂盒8和流式细胞术确定细胞增殖和凋亡。miR-217与Mafb之间的相关性已通过生物学软件进行了预测，并通过双重荧光素酶测定法得以证实。免疫印迹用于检测蛋白质表达。来自GEO数据库的数据显示，miR-217在T2DM患者中被上调。HG处理可上调miR-217的表达，抑制其增殖，并促进β-TC-tet细胞的凋亡和炎症反应。miR-217的消耗减轻了HG引起的β-TC-tet细胞损伤。黑手党被确认为miR-217的靶标，并且被miR-217负调控。敲除Mafb减弱了miR-217抑制剂对β-TC-tet细胞损伤的缓解作用。HG上调NF-κB信号通路中关键蛋白的表达，而miR-217抑制剂抑制这种上调趋势。此外，沉默Mafb可以减轻miR-217抑制剂对这些蛋白质的抑制作用。我们的发现表明，抑制miR-217可通过调节Mafb和NF-κB信号传导减轻HG诱导的β-TC-tet损伤。