Effect of lipopolysaccharide on stimulating high mobility group box-1 protein expression in peritoneal macrophages in rats and its potential signaling mechanism
- VernacularTitle:大鼠腹腔巨噬细胞高迁移率族蛋白B1诱生机制的初步探讨
- Author:
Hui LIU
;
Yongming YAO
;
Yan YU
- Publication Type:Journal Article
- Keywords:
macrophages;
endotoxins;
high mobility group box-1 protein;
Janus kinase/signal transducer and activator of transcription pathway;
signal transduction
- From:
Medical Journal of Chinese People's Liberation Army
1982;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of lipopolysaccharide (LPS) on stimulating high mobility group box-1 protein (HMGB1) mRNA expression in peritoneal macrophages in rats and its potential signaling mechanism. Methods Abdominal macrophages obtained from male Wistar rats were seeded on 24-well (1?10 6 cells/well) tissue culture plates. The cells were incubated for 3 days before they were stimulated with LPS, fludarabine (specific inhibitor of signal transducer and activator of transcription 1, STAT1), or rapamycin (specific inhibitor of signal transducer and activator of transcription 3, STAT3). After being stimulated, macrophages were denatured directly in tissue culture plates to determine HMGB1 mRNA expression. The time-dependent and dose-dependent responses between LPS stimulation and HMGB1 mRNA expression were analyzed, and the effect of treatment with fludarabine and rapamycin on HMGB1 mRNA expression was also observed. Results After being stimulated with 75-100ng/ml LPS, the HMGB1 mRNA expressions in macrophages were up-regulated markedly, peaking at 24-36 hours, and remained elevated up to 48 hours. It was found that the HMGB1 mRNA expression was significantly inhibited by treatment with either fludarabine (100?mol/L) or rapamycin (25ng/ml). Conclusions These data suggest that LPS stimulation can result in up-regulation of HMGB1 mRNA expression in peritoneal macrophages in rats. Janus kinase/STAT pathway may be involved in modulating HMGB1 mRNA expression in LPS-activated macrophages.