MAPK信号通路参与调控大鼠腹腔巨噬细胞表达CRH

MAPK signal pathway participates the regulation of expression of corticotropin-releasing hormone in rat peritoneal macrophages

为了解终末巨噬细胞表达促肾上腺皮质激素释放激素(CRH)的胞内信号转导机制,明确丝裂原活化蛋白激酶(MAPK)信号通路与脂多糖(LPS)诱导的大鼠腹腔表达CRH的关系。我们利用体外培养的大鼠腹腔巨噬细胞,采用RT-PCR及ELISA方法观察MAPK信号通路中关键激酶特异性阻断剂(PD98059、SB203580、SP600125)对LPS诱导的CRH表达的影响。结果显示,LPS促进了大鼠腹腔巨噬细胞表达CRH,MAPK三条主要信号通路中关键激酶特异性阻断剂均剂量依赖性地抑制了LPS诱导的CRH表达。因此,我们认为LPS可以促进终末巨噬细胞表达CRH,而MAPK信号通路参与了该过程。

To understand the mechanism of intracellular signal transduction to express the corticotropin-releasing hormone （CRH） in the terminal macropbages and the relationship between mitogen-activated protein kinase（MARK）signal pathway and the expression of CRH in peritoneal macrophages induced by I.PS, the peritoneal macrophages harvested from Wistar rats were cultivated in DMEM medium with 10% fetal bovine serum, and the effect of MARK signal pathway-specific blockers PD98059, SB203580 and SP600125 on the expression of CRH induced by LPS in the cultured cells was determined by RT-PCR and ELISA assay. It was found that LPS could enhance the expression of CRH in rat peritoneal macrophages, and all the blockers used could inhibit the effect of LPS in dose-dependent manner. It is evident that I.PS can improve the expression of CRH in terminal maerophages and MARK signal pathway participates this process.