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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 (endotoxicshock ,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 (p38mitogen acti vatedproteinkinase ,p38MAPK)的信号转导作用。用生理多道记录仪观察尾静脉注入LPS (8mg/kgi v )复制的SD大鼠ES模型、LPS注入前 10min尾静脉注入CCK 8(40 μg/kgi v )、单独注入CCK 8(40 μg/kgi 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Westernblot检测肺脏p38MAPK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p38MAPK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
To investigate the effects of cholecystokinin octapeptide (CCK 8) on the changes of serum and lung cytokines in rats during endotoxic shock (ES) induced by lipopolysaccharide (LPS), and to investigate the effect of p38 mitogen-activated P38 mitogen acti vated protein kinase (p38MAPK) signal transduction. Sprague-Dawley rats were injected with LPS (8mg / kg iv) into the caudal vein. CCK 8 (40 μg / kg iv) was injected into the caudal vein 10 min before LPS injection. CCK 8 (40 μg / The changes of mean arterial pressure (MAP) in the four groups of rats were measured by ELISA, and the changes of inflammatory cytokines (TNFα, IL 1β and IL 6) in serum and lungs were detected. The lung p38MAPK expression was detected by Western blot. The results showed that: CCK 8 can improve LPS-induced decreased MAP in rats. Compared with the control group, LPS can significantly increase the serum and lung TNFα, IL 1β and IL 6 content; CCK 8 can significantly inhibit LPS-induced serum and lung TNFα, IL 1β and IL 6 increased. CCK 8 increased phosphorylated p38MAPK expression in the lungs of ES rats. The results suggest that CCK 8 can reduce the MAP in ES rats and inhibit the overproduction of proinflammatory cytokines in the lung, and p38MAPK may be involved in its signal transduction mechanism