Lipopolysaccharide-enhanced early proliferation of insulin secreting NIT-1 cell is associated with nuclear factor-kappaB- mediated inhibition of caspase 3 cleavage / 中华医学杂志(英文版)
Chinese Medical Journal
; (24): 3652-3656, 2011.
Article
in En
| WPRIM
| ID: wpr-273997
Responsible library:
WPRO
ABSTRACT
<p><b>BACKGROUND</b>Increased levels of plasma lipopolysaccharide (LPS) have been found in obesity and diabetes patients. This study was to investigate the effect of LPS on pancreatic beta-cell viability and the involvement of caspase 3 in NIT-1 cell line.</p><p><b>METHODS</b>Mouse insulinoma NIT-1 cells were treated with LPS for the indicated time and dose. Cell viability was measured by cell counting kit-8 reagent. Toll-like receptor 4 (TLR4), caspase 3 and cleaved caspase 3 were detected by Western blotting. Insulin was determined by radioimmunoassay (RIA).</p><p><b>RESULTS</b>LPS promoted NIT-1 cell proliferation at 1 µg/ml, peaked at 72 hours of incubation. A reduction in cleavage of caspase 3 was observed upon LPS treatment. Bay11-7082, a specific inhibitor of nuclear factor (NF)-κB, blunted LPS-induced inhibition of caspase 3 cleavage. Reduction in chronic insulin secretion was observed after treatment with LPS at 1 µg/ml for 48 and 72 hours, not for 24 hours. TLR4 protein was upregulated when NIT-1 cells were treated with LPS at 1 µg/ml for 24 hours.</p><p><b>CONCLUSIONS</b>LPS promotes early NIT-1 cell proliferation in association with NF-κB-mediated inhibition of caspase 3 cleavage. LPS exerts a time-dependent inhibitory effect on chronic insulin secretion from NIT-1 cells.</p>
Full text:
1
Database:
WPRIM
Main subject:
Pharmacology
/
Lipopolysaccharides
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NF-kappa B
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Bodily Secretions
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Cell Line, Tumor
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Cell Proliferation
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Toll-Like Receptor 4
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Caspase 3
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Insulin
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Insulinoma
Limits:
Animals
Language:
En
Journal:
Chinese Medical Journal
Year:
2011
Document type:
Article