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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100μg/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 AG490、氟达拉滨的影响。结果:脂多糖诱导BRL-3A细胞24h后HMGB1 mRNA表达水平和培养上清液中HMGB1含量明显升高(P<0.01),25μmol/L tyrphostin AG490和50μmol/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。
AIM: To investigate the role of Janus kinase / signal transducer and activator of transcription (JAK / STAT) signaling pathway in the release of high mobility group box-1 (HMGB1) from hepatocytes induced by lipopolysaccharide (LPS). Methods: The expression of HMGB1 mRNA in rat hepatocytes BRL-3A cells and the content of HMGB1 in the cell culture supernatant of 100μg / L lipopolysaccharide were determined. The effects of different concentrations of JAK / STAT inhibitor tyrphostin AG490, Rabin’s influence. Results: The expression of HMGB1 mRNA and the content of HMGB1 in culture supernatant of BRL-3A cells were significantly increased after lipopolysaccharide treatment (P <0.01), while those of 25 μmol / L tyrphostin AG490 and 50 μmol / L fludarabine on these two indexes Showed a certain degree of inhibition (P <0.05). Conclusion: Lipopolysaccharide (LPS) can induce the expression and release of HMGB1 in hepatocytes, which may be related to the JAK / STAT signaling pathway.