Resistin基因对胰岛β细胞RINm5F增殖的影响

Resistin inhibits rat insulinoma cell RINm5F proliferation

目的Resistin被认为是联系肥胖与2型糖尿病的脂肪因子。本研究旨在探讨resistin基因过表达对胰岛β细胞株RINm5F增殖的影响。方法体外培养RINm5F大鼠胰岛β细胞,通过pcDNA3.1-resistin真核表达质粒转染RINm5F细胞,筛选稳定表达株。采用四甲基偶氮唑盐(MTT)法检测细胞增殖,采用RT-PCR法验证Resistin mRNA水平及检测SOCS-3的mRNA水平,Western blot法检测Akt的总蛋白和磷酸化水平。结果过表达resistin的RINm5F细胞增殖速度显著低于正常对照组(P<0.05)。过表达resistin的RINm5F细胞中Akt磷酸化水平为正常对照组的0.6倍(P<0.05),而SOCS-3mRNA水平为正常对照组的3.2倍(P<0.05)。结论Resistin基因过表达减缓了胰岛β细胞RINm5F的增殖,其机制可能与上调了SOCS-3从而导致Akt下调有关。

Objective Resistin was thought to link the obesity to type 2 diabetes. This study aimed to investigate the effect of resistin on insulinoma cell proliferation. Methods pcDNA3. 1-resistin was transfeeted into rat insulinoma cells RINm5F. Cell proliferation was assessed by the MTT assay. The resistin and SOCS3 mRNA levels were assessed by RT-PCR. The total Akt level and the phosphorylation status were assessed by Western blot. Results The over-expressed resistin inhibited the RINm5F cell proliferation （ P 〈 0. 05 ）. SOCS-3 expression was up-regulated by resistin overexpression （3.2 folds over the control; P 〈 0.05 ）. Akt phosphorylation was down-regulated by resistin over-expression （0.6 fold over the control ; P 〈 0.05 ）. Conclusions Resistin impairs the rat insulinoma cell RINm5 F proliferation. This might be attributed to a down-regulation of Akt level caused by increased SOCS-3 expression.