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[目的]探讨促肾上腺皮质激素释放激素(corticotropin releasing hormone,CRH)家族在人类胎盘滋养细胞中核转录因子κB(nuclear factor-kappa B,NF-κB)和丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPK)炎症信号通路中的作用.[方法]使用CRH,UCN,UCN2和UCN3处理人胎盘滋养层细胞系Jeg-3细胞,并使用CRH-受体拮抗剂与CRH家族共孵育Jeg-3细胞,采用Western blot评估CRH家族对NF-κB蛋白表达及对抑制蛋白IκB和MAPK磷酸化的影响.[结果]Jeg-3细胞经过CRH处理后,p38MAPK的磷酸化程度显著升高;Jeg-3细胞经UCN2处理后,NF-κB蛋白表达显著升高,IκB和MAPK磷酸化程度显著升高;而经过CRH-受体拮抗剂处理后,NF-κB和MAPK通路被抑制;UCN和UCN3对NF-κB和MAPK通路无影响.[结论]在人类胎盘滋养层细胞的炎症过程中,UCN2参与激活NF-κB和MAPK信号通路的促炎神经肽,而CRH是参与激活MAPK信号通路的促炎神经肽,CRH和 UCN2可能参与了妊娠和分娩的发动机制.“,”[Objective]To investigate the role of corticotropin-releasing hormone(CRH)family in the in-flammatory signaling pathways of nuclear factor κB(NF-κB)and mitogen-activated protein kinase(MAPK)in human placental trophoblast.[Methods]Human placental trophoblastic cell line Jeg-3 cells were treated with CRH,UCN,UCN2and UCN3.CRH-receptor antagonists were used to co-incubate Jeg-3 cells with CRH fami-ly.Western blot was used to evaluate the expression of NF-κB by CRH family and the effects on phosphoryla-tion of IκB and MAPK.[Results]The phosphorylation of p38 MAPK in Jeg-3 cells was significantly increased after CRH treatment.After Jeg-3 cells were treated with UCN2,the expression of NF-κB protein increased significantly,and the phosphorylation of IκB and MAPK increased significantly.After treatment with CRH-receptor antagonists,the NF-κB and MAPK pathway were inhibited.UCN and UCN3 had no effect on NF-κB and MAPK pathway.[Conclusion]UCN2 is involved in the activation of inflammatory neuropeptides of NF-κB and MAPK signaling pathway during inflammation of human placental trophoblastic cells.CRH is an inflam-matory neuropeptide involved in the activation of the MAPK signaling pathway.CRH and UCN2 may be in-volved in the motor system for pregnancy and childbirth.