Effects of low-dose lipopolysaccharide on cell apoptosis, proliferation, and insulin secretion in NIT-1 β-cells
10.3760/cma.j.issn.1000-6699.2011.09.015
- VernacularTitle:低剂量脂多糖对NIT-1β细胞凋亡、增殖和分泌功能的影响
- Author:
Qijun LIANG
;
Yan LI
;
Shanying LIU
;
Ying LIANG
;
Li YAN
;
Zuzhi FU
- Publication Type:Journal Article
- Keywords:
Lipopolysaccharide;
NIT-1 β-cell;
Apoptosis;
Proliferation;
Insulin secretion
- From:
Chinese Journal of Endocrinology and Metabolism
2011;27(9):761-765
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effects of lipopolysaccharide ( LPS ) on cell apoptosis,proliferation, and insulin secretion in a β-cell line, NIT-1. MethodsNIT-1 cells were stimulated with 1 μg/ml LPS for 0-120 h. Cell apoptosis was evaluated by Hochest33342 staining and Annexin V/PI flow cytometry. Cell proliferation was evaluated by CCK-8 and BrdU assay. Intracellular insulin content, basal insulin secretion, and glucose-stimulated insulin secretion(GSIS) were detected by RIA. The IRS-2 tyrosine phosphorylation was determined by Western blot. ResultsCell apoptosis was not significantly changed by treatment with LPS for 120 h. Cell proliferation was stimulated by LPS before 48 h, and inhibited after 96 h. Intracellular insulin content or GSIS was not altered, but basal insulin secretion was decreased significantly by LPS after 48 h ( all P＜0.01 ). LPS decreased the tyrosine phosphorylation level of IRS-2 ( 0. 45 ± 0. 08 vs 0. 22 ± 0. 06, P ＜ 0. 05 ) and stimulated IκBα phosphorylation. Pretreatment with a specific IκBα phosphorylation inhibitor, Bay1 1-7082 for 1 h, remarkably blunted the LPS-induced phosphorylation of IκBα and cell proliferation( both P＜0.01 ). ConclusionsLow-dosages of LPS regulate proliferation and basal insulin secretion of NIT-1 β-cells, in which activation of NF-κB and inhibition of IRS2 tyrosine-phosphorylation may be involved.
