Effect of JAK/STAT signaling pathway on extracellular release of HMGB1 in lipopolysaccharide-induced hepatocytes
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摘要:
目的:探讨Janus激酶/信号转导和转录激活子(JAK/STAT)信号通路在内毒素脂多糖诱导肝细胞高迁移率族蛋白B1(HMGB1)释放中的作用-方法:观察100 μg/L 脂多糖诱导后,大鼠肝细胞BRL-3A细胞HMGB1 mRNA表达水平和细胞培养上清液中HMGB1含量的变化,及不同浓度的JAK/STAT通路抑制剂tyrphostin AG 490-氟达拉滨的影响-结果:脂多糖诱导BRL-3A细胞24 h后HMGB1 mRNA表达水平和培养上清液中HMGB1含量明显升高(P < 0.01),25 μmol/L tyrphostin AG 490和50 μmol/L氟达拉滨对以上2个指标显示一定程度的抑制作用(P < 0.05)-结论:内毒素脂多糖可诱导肝细胞HMGB1的表达和释放,其机制可能与细胞JAK/STAT信号通路有关-
Abstract:
Objective:To study the effect of JAK/STAT signaling pathway on extracellular release of high mobility group box 1 (HMGB1) in endotoxin-induced hepatocytes. Methods:HMGB1 concentration was determined in the culture medium of 100 μg/L lipopolysaccharide-induced BRL-3A hepatocytes by enzyme-linked immunosorbent assay (ELISA),and the change of HMGB1 mRNA expression was detected by RT-PCR method. The effects of JAK/STAT pathway inhibitors (tyrphostin AG 490 and fludarabine) with various concentrations on HMGB1 mRNA expression and extracellular release were investigated. Results:The level of HMGB1 mRNA expression and HMGB1 concentration in the culture medium significantly increased after BRL-3A hepatocytes induced by lipopolysaccharide for 24 hours(P < 0.01). 25 μmol/L tyrphostin AG 490 and 50 μmol/L fludarabine partly inhibited HMGB1 mRNA expression and extracellular release in lipopolysaccharide-induced BRL-3A hepatocytes(P < 0.05). Conclusion:Lipopolysaccharide induces hepatocytes to release HMGB1,which is related to intracellular JAK/STAT signaling pathway.
