摘要
目的 :观察溃疡性结肠炎患者 PMN凋亡的变化 ,探讨细胞因子对 PMN凋亡的影响。方法 :检测 2 8例 UC病人外周血 PMN凋亡和细胞因子及粘附分子水平。结果 :活动期 UC患者 PMN凋亡率明显低于健康人对照组和缓解期 UC患者。缓解期 UC患者 PMN凋亡率与对照组无差别。不同病情活动期 UC患者 PMN凋亡有显著性差异。活动期 UC患者外周血中 IL - 8、IL- 6、TNF-α、NO、P- sel、ICAM- 1水平均高于对照组和缓解组 ,且与 PMN凋亡呈负相关 ,与病情呈正相关。缓解组患者 IL- 8、IL- 6、TNF- α、NO、P- sel和 ICAM- 1与对照组无显著性差异。结论 :UC患者 PMN凋亡延迟 ,且与病情及疗效密切相关。各种炎性细胞因子产生过多、各种免疫细胞粘附分子表达上调可能是导致 PMN凋亡延迟的重要机制。适度调控 PMN凋亡 ,有可能会成为治疗 UC的有效途径。
Objective: To observe the changes o f neutrophils (PMN) apoptosis and the levels of inflammatory cytokines and adhesion molecules in patients with ulcera tive colitis (UC) and to study the relationship between them. Methods: The apop tosis of neutrophil in 28 patients with UC at the active stage and 13 patients w ith UC at the remission stage were determined with flow cytometry. The inflammat ory cytokines and the adhesion molecules were tested with ELISA method. Results: The percentage of neutrophil apoptosis in the patients with UC at the active st age was obviously lower than that of healthy persons and the patients with UC at the remission stage. There were no differential significance of neutrophil apop tosis between healthy persons and patients with UC at remission stage. Significa nt differences in apoptosis of neutrophils were found among the different clinic al stages of active UC patients. The levels of IL-8, TNF-α, IL-6 , NO, P-s el and ICAM-1 in patients with UC at the active stage were significantly,higher than that of healthy persons and the patients with UC at the remission stage and the increasing levels of inflammatory cytokins and adhesion molecules in ac tive UC patients wer e negatively correlated to the percentage of neutrophil apoptosis and positively correlated to the severity of UC. Conclusion: The data demonstrated a delay in apoptotic process of neutrophils in active UC. The high expression of inflammato r y cytokines and adhesion molecules may play an important role in the cause of in hibition of neutrophil apoptosis which prolongs the functional life span of neut rophil. Therefore the delayed apoptotic neutrophils produce more inflammatory me diators participating in the damage of colonic tissue.Adjusting the expression of cytokines and adhesion molecules and moderately controlling th e apoptosis of neutrophils further may be a new therapeutic target for UC.
出处
《陕西医学杂志》
CAS
北大核心
2004年第12期1069-1072,共4页
Shaanxi Medical Journal
基金
广东省湛江市科技攻关项目 (ZK0 1 2 3 )
