Li Shujin, Cong Bin, Yan Yunli, Yao Yuxia, Ma Chunling, Ling Yiling
Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China.
Chin Med J (Engl). 2002 Feb;115(2):276-9.
To study the effect of cholecystokinin octapeptide (CCK-8) on lipopolysaccharide (LPS)-stimulated pulmonary interstitial macrophages (PIM) in vitro.
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.
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.
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.
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。
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）。
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。
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。
