中文摘要：

目的：观察八肽胆囊收缩素（CCK-8）对脂多糖诱导小鼠分泌IL-12的影响，探讨核因子-κB（NF—κB）和p38丝裂原活化蛋白激酶（p38 MAPK）的信号转导作用。方法：雌性BALB／c小鼠经LPS诱导后分别给予CCK及CCK—A、B受体拮抗剂。ELISA法检测小鼠血清及肺、脾组织中IL-12p40、p70的表达；Western blotting法检测肺脏、脾脏IKB、p38MAPK的表达；EMSA法检测肺、脾组织中NF—κB／DNA的结合活性。结果：CCK-8进一步提高了LPS诱导的小鼠血清及肺、脾组织中IL-12p40、p70的表达；抑制IKB磷酸化和NF-κB／DNA结合活性；促进p38MAPK磷酸化。而CCK—A受体拮抗剂（CR-1409）及CCK—B受体拮抗剂（CR-2945）部分逆转了CCK-8的效应。结论：CCK-8可促进LPS诱导小鼠分泌IL-12，p38MAPK可能参与了其信号转导机制，而NF—KB途径可能并未参与CCK-8促IL-12分泌这一过程。

英文摘要：

AIM： To study the effects of CCK -8 on IL - 12 secretion in LPS - induced mice and to investigate the signal transduction mechanisms involving NF - κB and p38 MAPK. METHODS： Female BALB/c mice were induced by LPS in the presence or absence of CCK - 8, CCK - A or B receptor antagonist. The productions of IL - 12p40 and p70 in the sera, lung and spleen tissues were evaluated by ELISA. Changes of plκB, p - p38 protein expression and the NF - κB/DNA binding activity were examined by Western blotting and EMSA, respectively. RESULTS： CCK - 8 increased the expressions of IL- 12p40, p70 in the serum, lung and spleen tissues of LPS - induced mice, inhibited IκB phosphorylation and NF- κB/DNA binding activity, increased p38 phosphorylation. CONCLUSION： CCK -8 increases the production of IL - 12 in LPS - induced mice probably via activating p38 MAPK. NF - κB might not mediate the activating effect of CCK - 8 on IL - 12 production.