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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。
Objective To investigate the effect of octapeptide cholecystokinin (CCK 8) on the expression of inducible nitric oxide synthase (iNOS) in vascular endothelial cells induced by lipopolysaccharide (LPS). Methods Human umbilical vein endothelial cell line ECV 304 was cultured and treated with 0.01, 0.1 and 1 mg / L LPS for 2-24 h. The cells were treated with normal saline, 1-0 7mol / L CCK 8 and 0.1 mg / L LPS + 1- 0, 1, 0, 1, 10-8mol / L CCK 8 for 16 h. The content of nitric oxide (NO), the activity of NO in culture medium, the immunocytochemistry and Western blotting were detected by colorimetric method iNO S protein expression. Results Compared with the saline control group, the NO content in LPS-induced medium increased and the activity of NO S increased. The expression of iNO S protein was up-regulated. CCK 8 inhibited the above-mentioned effects of LPS in a dose-dependent manner, NO S activity and NO content had no significant effect. Conclusion CCK 8 can significantly inhibit LPS-induced up-regulation of iNO S protein expression in ECV 304 cells and decrease NO production.