摘要目的 观察乌司他丁对重症急性胰腺炎(Severe acute panereatitis,SAP)大鼠脾淋巴细胞功能的影响.方法 清洁级Wistar大鼠28只随机分为对照组、假手术组、SAP组和乌司他丁组.对照组不施行手术,假手术组不给予胆胰管内注入脱氧胆酸钠,余同SAP模型组.乌司他丁组在制作SAP模型后30min经尾静脉注射乌司他丁5万U/kg,其他3组均注入等量生理盐水.术后24 h处死大鼠.分离培养脾淋巴细胞,MIT法检测脾淋巴细胞增殖活性,ELISA法检测脾淋巴细胞培养上清中Th1细胞因子IL-2、IFN-γ和Th2细胞因子IL-10水平.计量资料以均数±标准差(x±s)表示,采用SPSS 10.0统计软件包进行数据处理.组间比较采用Student't检验.以P＜0.05为差异具有统计学意义.结果 与假手术组相比,SAP组脾淋巴细胞增殖活性明显下降,Th1和Th2细胞因子产生均明显减少.与SAP组相比,乌司他丁组脾淋巴细胞增殖活性明显升高,Th1和Th2细胞因子生成也明显增加.结论 SAP脾淋巴细胞增贿障碍,且Th1/Th2平衡失调,应用鸟司他丁有助于改善脾淋巴细胞功能异常,减轻SAP特异性免疫功能障碍.

abstractsObjective To investigate the effects of Ulinastatin(UTI)on the function of splenic lymphocytes from rats with severe acute pancreatitis(SAP).Method Twenty-eight Wister rats(clean grade)were randomly divided into control,sham operation,SAP,and ulinastatin group.No operation was performed in control group.And rats with sham-operation received laparotomy and catheterization into choledocho-pancreatic duct without injection of sodium deoxycholic.Rats in ulinastatin group received ulinastatin injection(50000 U/kg)via tail vein 30 minutes after pancreatitis induced with DCA injected into pancreatic duct.Rats ofother groups were given equal volume of saline.At 2,4 hours after operation,all animals were killed by neck dislocation,and splenocytes were isolated and cultured in RPMI 1640 medium containing 10%fetal calf serum.Proliferation of splenecytes was determined with MIT cellular proliferation assay.Levels of Th1 cytokines(IL-2,IFN-γ)and Th2 cytokine(IL-10)in supematants of splenoeytesweremeasured by ELISA.Quantitative data were expressed as mean±SE.Statistical analyses were performed by Student's t test with SPSS software(version 10.0 for Windows).A P value less than 0.05 Was considered statistically significant. Results The concentration of IL-2, IL-10 and IFN-γ and proliferative activity of splenocytes in SAP group were significantly lower than that in sham operation group.In contrast,the proliferative as well as the eytokine-releasing capacities of the solenecms from rats treated with UTI were significantly increased compared with those from rats with SAP.Conclusions The deficiencies in proliferation and cytokine release in response to antigen stimulation inaplys an anergic state of splenocytes during SAP.Treatment with UTI contributed to the recovery of the immune function by improving proliferative responses and cytokine release of splenocytes.