核转录因子-κB在高浓度葡萄糖诱导INS-1细胞凋亡中的作用  

High glucose induces INS-1 cell apoptosis by activating nuclear factor-κB

作　　者：张巧玲[1] 薛耀明[1] 朱波[1] 李佳[1] 沙建平[1] 李圣坚[1] 

机构地区：[1]南方医科大学南方医院内分泌科,广东广州510515

出　　处：《南方医科大学学报》2010年第10期2307-2309,共3页Journal of Southern Medical University

基　　金：广东省中医药局课题(2009454);广东省科技计划项目(2009B080701020)

摘　　要：目的研究核转录因子(NF-κB)在高浓度葡萄糖诱导INS-1细胞凋亡中的作用。方法大鼠胰岛素瘤细胞系(INS-1)细胞以RPMI1640培养基常规培养。实验分对照组(11.1mmol/l葡萄糖组)、高糖组(33.3mmol/l葡萄糖组)、高糖+NF-κB抑制剂组(33.3mmol/l葡萄糖+NF-κB抑制剂(5μmol/l)干预组)3组。以荧光定量RT-PCR检测IKKβ mRNA水平,Western blot法检测细胞核内NF-κB亚基P65蛋白表达量,Annexin V-PI双染法检测细胞凋亡率。结果与对照组相比较,高糖组IKKβ mRNA水平显著升高(P<0.01),INS-1细胞胞核内P65蛋白表达显著增多(P<0.01),细胞凋亡率显著升高(P<0.05)。与高糖相比较,高糖+NF-κB抑制剂组IKKβ mRNA水平显著下降(P<0.01),胞核内P65蛋白表达显著减少(P<0.01),INS-1细胞凋亡率显著下降(P<0.05)。结论高浓度葡萄糖诱导INS-1细胞NF-κB活化,抑制NF-κB活化可有效抑制高糖诱导的INS-1细胞凋亡。Objective To study of the role of nucleartranscription factor-kB（NF-kB） in high glucose-induced apoptosis in INS-1 cells.Methods Rat insulinoma（INS-1） cells cultured in RPMI 1640 medium were treated with 11.1 mmol/L glucose,33.3 mmol/L glucose,or 33.3 mmol/L glucose plus 5 kBol/L NF-kB inhibitors for48 h.The expression of NF-kB subunit P65 protein in the cell nuclei was detected by Western blotting,IKK？ mRNA level by quantitative RT-PCR,and cell apoptosis by Annexin V-PI double staining.Results Compared with the control levels,IKK？ mRNA levels of the cells significantly increased in response to 33.3 mmol/L glucose exposure（P0.01）,which also resulted in significantly increased P65 protein expression in the cell nuclei（P0.01） and cell apoptosis rate（P0.05）.Compared with those in the high glucose group,the expression of IKK？ mRNA and P65 protein and cell apoptosis rate decreased significantly after treatment with 33.3 mmol/L glucose plus 5 kBol/L NF-kB inhibitors（P0.05）.Conclusion High glucose induces NF-kB activation in INS-1 cells,and inhibition of NF-kB activation may protect INS-1 cells from high glucose-induced cell apoptosis.

关 键 词：高浓度葡萄糖 INS-1细胞 NF—kaapaB P65 

分 类 号：R587.1[医药卫生—内分泌]