Cholecystokinin octapeptide inhibits the in vitro expression of CD14 in rat pulmonary interstitial macrophages induced by lipopolysaccharide  

八肽胆囊收缩素抑制脂多糖诱导的大鼠肺间质巨噬细胞CD14的表达(英文)

作　　者：李淑瑾[1] 丛斌[1] 阎蕴力[2] 姚玉霞[3] 马春玲[3] 凌亦凌[1] 

机构地区：[1]河北医科大学病理生理教研室,河北石家庄050017 [2]河北医科大学基础所细胞生物室,河北石家庄050017 [3]河北医科大学实验动物中心分子生物学研究室,河北石家庄050017

出　　处：《Chinese Medical Journal》2002年第2期276-279,共4页中华医学杂志（英文版）

基　　金：HebeiNaturalScienceFoundation (No 30 0 32 2 )

摘　　要：OBJECTIVE: To study the effect of cholecystokinin octapeptide (CCK-8) on lipopolysaccharide (LPS)-stimulated pulmonary interstitial macrophages (PIM) in vitro. METHODS: PIM were isolated and cultured in the presence or absence of LPS, CCK-8, proglumide (the antagonist of CCK receptors) and vehicle. The expression of membrane CD14 (mCD14) protein was assayed by flow cytometry and soluble CD14 (sCD14) in the supernatant was analyzed semi-quantitatively by Western blot. TNF-alpha in the supernatant was detected with ELISA. RESULTS: CCK-8, at concentrations of 10(-7) mol/L and 10(-6) mol/L, significantly inhibited the expression of mCD14. Release of sCD14 and TNF-alpha in the supernatant was up-regulated by LPS (1 microg/ml) but reduced by CCK-8. The effect of CCK-8 was inhibited by proglumide. CONCLUSION: CCK-8 negatively modulated several functions of LPS-stimulated PIM through CCK receptors. This may be one of the mechanisms for CCK-8 to alleviate inflammation in lung tissue during endotoxemia.目的　初步探讨八肽胆囊收缩素 (CCK 8)对体外脂多糖 (LPS)激活大鼠肺间质巨噬细胞 (PIM)的调节作用。方法　分离大鼠肺PIM ,经LPS、CCK 8、CCK受体拮抗剂丙谷胺及溶剂单独或共同孵育后 ,测定细胞CD14的表达及上清液中TNF α的含量。结果　LPS(1mg/L)孵育 12小时 ,肺PIMmCD14表达上调 ,上清中sCD14及TNF α含量均明显增加 ;CCK 8(10 7-10 6mol/L)抑制了LPS的上述效应 ,并可被丙谷胺所拮抗。结论　CCK 8对LPS激活的肺PIM的部分功能具有抑制性调节作用 ,该作用是由其受体介导的 ,可能是CCK 8减轻内毒素血症时肺组织炎性变化的重要机制之一。

关 键 词：Animals Antigens  CD14 Cells  Cultured Culture Media  Conditioned Female Lipopolysaccharides Macrophages  Alveolar RATS Rats  Sprague-Dawley Research Support  Non-U.S. Gov't SINCALIDE Specific Pathogen-Free Organisms Tumor Necrosis Factor-alpha 

分 类 号：R563.9[医药卫生—呼吸系统]