【摘要】 目的探讨八肽缩胆囊素(CCK 8)对脂多糖(LPS)诱导血管内皮细胞诱生型一氧化氮合酶(iNO S)表达变化的影响。方法培养人脐静脉内皮细胞株ECV 304细胞,用0.01、0.1和1 m g/L LPS处理2~24 h,用生理盐水、1-0 7m o l/L CCK 8和0.1 m g/L LPS+1-0 6、1-0 7、10-8m o l/L CCK 8处理16 h;用比色法检测培养液中一氧化氮(NO)含量、细胞NO S活性,免疫细胞化学及蛋白质免疫印迹法检测iNO S蛋白表达。结果与生理盐水处理的对照组比较,LPS诱导培养液NO含量增多、细胞NO S活性增高、iNO S蛋白表达上调;CCK 8剂量依赖性抑制LPS的上述效应,而单独作用对iNO S蛋白表达、NO S活性和NO含量均无明显影响。结论CCK 8可以明显抑制LPS引起ECV 304细胞iNO S蛋白表达上调,减少NO生成。更多还原

【Abstract】 Objective To investigate the effect of cholecystokinin octapeptide（CCK8） on lipopolysaccharide（LPS）elicited inducible nitric oxide synthase（iNOS） expression in vascular endothelial cells.Methods Human umbilical vein endothelial cell line（ECV304 cells） was stimulated with vehicle（normal saline） or LPS in the presence（0.01,0.1,1 mg/L） or absence（0.1 mg/L） of CCK8((10^-6-10^-8 mol/L)). Nitric oxide（NO） level and cellular nitric oxide synthase（NOS） activity were （determined） with spectrophotometrically. The iNOS expression was detected with immunocytochemical（technique） and Western blot.Results Compared with normal saline,LPS significantly induced the（upregulation） of iNOS protein expression in the cultured ECV304 cells,and NOS activity in ECV304 cells and NO level in cultured media were increased.CCK8（obviously） inhibited abovementioned effect of LPS in a dosedependent manner.Whereas CCK8（alone） did not showed effect on iNOS protein expression,NO level and cellular NOS activity as compared with those values when vehicle was used.Conclusion CCK8 inhibite LPSelicited iNOS expression and NO production in ECV304 cells.更多还原