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

ABSTRACT

OBJECTIVE: To study of the role of nuclear transcription factor-κB (NF-κB) 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 µmol/L NF-κB inhibitors for 48 h. The expression of NF-κB subunit P65 protein in the cell nuclei was detected by Western blotting, IKK belta mRNA level by quantitative RT-PCR, and cell apoptosis by Annexin V-PI double staining. RESULTS: Compared with the control levels, IKK belta mRNA levels of the cells significantly increased in response to 33.3 mmol/L glucose exposure (P<0.01), which also resulted in significantly increased P65 protein expression in the cell nuclei (P<0.01) and cell apoptosis rate (P<0.05). Compared with those in the high glucose group, the expression of IKK belta mRNA and P65 protein and cell apoptosis rate decreased significantly after treatment with 33.3 mmol/L glucose plus 5 µmol/L NF-κB inhibitors (P<0.05). CONCLUSION: High glucose induces NF-κB activation in INS-1 cells, and inhibition of NF-κB activation may protect INS-1 cells from high glucose-induced cell apoptosis.