High glucose induces INS-1 cell apoptosis by activating nuclear factor-κB / 南方医科大学学报
Journal of Southern Medical University
;
(12): 2307-2309, 2010.
Artigo
em Chinês
| WPRIM
| ID: wpr-323674
ABSTRACT
<p><b>OBJECTIVE</b>To study of the role of nuclear transcription factor-κB (NF-κB) in high glucose-induced apoptosis in INS-1 cells.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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.</p>
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WPRIM (Pacífico Ocidental)
Assunto principal:
Neoplasias Pancreáticas
/
Patologia
/
Regulação da Expressão Gênica
/
Apoptose
/
Linhagem Celular Tumoral
/
Fator de Transcrição RelA
/
Glucose
/
Insulinoma
/
Metabolismo
Limite:
Animais
Idioma:
Chinês
Revista:
Journal of Southern Medical University
Ano de publicação:
2010
Tipo de documento:
Artigo
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