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目的:研究脂多糖(LPS)对肥大细胞高迁移率族蛋白B1(HMGB1)释放的诱导作用及其胞内信号通路。方法:采用小鼠肥大细胞株P815,观察不同剂量LPS诱导后细胞培养上清液中HMGB1含量和细胞HMGB1mRNA表达水平的变化,及不同剂量丝裂原活化蛋白激酶(MAPK)信号通路抑制剂(SB203580、SB202190、U0126和PD98059)对LPS诱导后HMGB1胞外释放的影响。HMGB1含量采用酶联免疫吸附试验检测。结果:LPS诱导后细胞培养上清液中HMGB1含量明显升高,并与LPS剂量、诱导时间有关;100μg/LLPS分别诱导8、24、48h后,HMGB1mRNA表达水平明显增强(P<0.01);SB203580和SB202190对LPS诱导HMGB1释放有明显的抑制作用(P<0.05),但U0126和PD98059不显示抑制作用。结论:LPS诱导肥大细胞释放HMGB1,其释放机制与胞内p38MAPK信号通路有关。
Objective: To study the induction of lipopolysaccharide (LPS) on the release of HMGB1 and its intracellular signaling pathway. Methods: Mouse mast cell line P815 was used to observe the changes of HMGB1 and HMGB1 mRNA expression in cell culture supernatant induced by different doses of LPS, and the effects of different doses of mitogen-activated protein kinase (MAPK) signaling inhibitor (SB203580 , SB202190, U0126 and PD98059) on the release of HMGB1 after LPS induction. HMGB1 content by enzyme-linked immunosorbent assay. Results: The content of HMGB1 in the cell culture supernatant after LPS induction was significantly increased, which was related to the dose of LPS and the induction time. The expression of HMGB1 mRNA was significantly increased after treated with 100μg / LPS for 8,24,48h (P <0.01), while SB203580 And SB202190 significantly inhibited the release of HMGB1 induced by LPS (P <0.05), but U0126 and PD98059 did not show any inhibitory effect. CONCLUSION: LPS induces the release of HMGB1 by mast cells, and its release mechanism is related to the intracellular p38 MAPK signaling pathway.