摘要
目的探讨八肽胆囊收缩素(cholecystokinin-octopep-tide,CCK-8)对脂多糖(lipopolysaccharide,LPS)诱导小鼠骨髓来源的树突状细胞(bone marrow-derived dendritic cell,BM-DC)分泌IL-12的影响。方法应用免疫荧光技术观察BM-DC表面CCK受体表达情况,酶联免疫吸附(ELISA)方法检测CCK-8对LPS诱导BM-DC分泌IL-12的影响,Western blot技术检测CCK-8对LPS诱导BM-DC细胞p38MAPK磷酸化的影响。结果BM-DC表面存在CCK-1R和CCK-2R;CCK-8促进LPS对BM-DC表达IL-12的诱导作用呈剂量依赖性(10-10、10-8、10-6mol·L-1);并能增加其p38磷酸化水平;CCK的1、2受体拮抗剂CR1409或CR2945均可减弱CCK-8的此种效应。结论CCK-8剂量依赖性促进了LPS诱导BM-DC分泌的IL-12,该作用由CCK-1R和CCK-2R介导,可能是通过促进p38MAPK的磷酸化作用而实现的。
Aim To investigate the effects of cholecys- tokinin-octopeptide on IL-12 secreted in murine bone marrow-derived dendritic cells induced by lipopolysaccharide. Methods The CCK receptor subtypes were investigated by immunofluorescence in murine bone marrow-derived dendritic cells. Enzyme linked immunosorbent assay and Western blot were used to estimate the contents of IL-12 and p38MAPK activity. Results CCK-1R and CCK-2R were detected in BM-DC ;CCK-8 (at concentrations of 10^-10, 10^-8, 10^-6 mol · L^-1 ) could significantly increase the secretion of IL-12 in the LPS-induced DC, and LPS-activated p38MAPK activity in a dose-dependent manner. The effect of CCK-8 was reduced partially by CR1409 (a CCK-1R antagonist) and CR2945( a CCK-2R antagonist). Conclusion CCK-8 could dose-dependently increase the expressions of IL-12 in LPS-induced DC,probably by promoting p38MAPK activity and the effect was mediated by CCK1 and CCK2 receptors.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2008年第3期357-361,共5页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No30770839)
河北省自然科学基金资助项目(No2007000833)