胆囊收缩素八肽抑制脂多糖诱导的大鼠肺间质巨噬细胞中CD14的体外表达。
Cholecystokinin octapeptide inhibits the in vitro expression of CD14 in rat pulmonary interstitial macrophages induced by lipopolysaccharide.
作者信息
Li Shujin, Cong Bin, Yan Yunli, Yao Yuxia, Ma Chunling, Ling Yiling
机构信息
Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China.
出版信息
Chin Med J (Engl). 2002 Feb;115(2):276-9.
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
研究八肽胆囊收缩素（CCK-8）对脂多糖（LPS）刺激的体外肺间质巨噬细胞（PIM）的影响。
方法
分离并培养PIM，分别在有或无LPS、CCK-8、丙谷胺（CCK受体拮抗剂）及赋形剂的情况下进行培养。采用流式细胞术检测膜CD14（mCD14）蛋白的表达，并用蛋白质印迹法对上清液中的可溶性CD14（sCD14）进行半定量分析。采用酶联免疫吸附测定法检测上清液中的肿瘤坏死因子-α（TNF-α）。
结果
浓度为10^(-7)mol/L和10^(-6)mol/L的CCK-8可显著抑制mCD14的表达。LPS（1μg/ml）可上调上清液中sCD14和TNF-α的释放，但CCK-8可使其降低。丙谷胺可抑制CCK-8的作用。
结论
CCK-8通过CCK受体对LPS刺激的PIM的多种功能产生负性调节作用。这可能是CCK-8在内毒素血症期间减轻肺组织炎症的机制之一。
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