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Inhibitory effect of cholecystokinin-octapeptide on production of cytokines in the lung of endotoxic shock rats

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Author:
No author available
Journal Title:
ACTA PHYSIOLOGICA SINICA
Issue:
2
DOI:
10.3321/j.issn:0371-0874.2002.02.003
Key Word:
缩胆囊素;内毒素;细胞因子;肺脏;p38丝裂素活化蛋白激酶

Abstract´╝Ü 观察八肽胆囊收缩素(cholecystokinin-octapeptide,CCK-8)改善脂多糖(lipopolysaccharide,LPS)引起的大鼠内毒素性休克(endotoxic shock,ES)过程中血清及肺脏细胞因子的变化,探讨p38丝裂素活化蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)的信号转导作用.用生理多道记录仪观察尾静脉注入LPS (8 mg/kg i.v.)复制的SD大鼠ES模型、 LPS注入前10 min尾静脉注入CCK-8 (40 μg/kg i.v.)、单独注入CCK-8 (40 μg/kg i.v.) 或生理盐水(对照)的四组大鼠平均动脉血压(MAP)的改变,应用ELISA试剂盒检测血清和肺脏中炎性细胞因子(TNF-α、IL-1β和IL-6)的变化.用Western blot检测肺脏p38 MAPK的表达.结果显示:CCK-8可改善LPS 引起的大鼠MAP的下降.与对照组相比,LPS可显著增加血清和肺脏TNF-α、IL-1β和IL-6含量;CCK-8可显著抑制LPS诱导的血清和肺脏TNF-α、IL-1β和IL-6的增加.CCK-8可增加ES大鼠肺脏磷酸化p38 MAPK的表达.结果提示CCK-8可改善ES大鼠MAP的降低,并对肺脏促炎性细胞因子过量产生有抑制作用,p38MAPK可能参与了其信号转导机制.

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