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


CONCLUSIONS
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.
Department of Endocrinology, Nanfang Hospital, Southern Medical University, Guangzhou510515, China. qiaoling000@yahoo.com.cn
Qiao-ling
QL
Zhang
Yao-ming
YM
Xue
Bo
B
Zhu
Jia
J
Li
Jian-ping
JP
Sha
Sheng-jian
SJ
Li
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D045744:Cell Line, Tumor; D005786:Gene Expression Regulation; D005947:Glucose / Q000009:adverse effects* / Q000378:metabolism; D007340:Insulinoma / Q000473:pathology*; D010190:Pancreatic Neoplasms / Q000473:pathology*; D051381:Rats; D051996:Transcription Factor RelA / Q000378:metabolism*
C498145:Rela protein, rat; D051996:Transcription Factor RelA; D005947:Glucose