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手术创伤对胸部肿瘤患者血清白细胞介素2受体、白细胞介素6和肿瘤坏死因子α表达的影响 被引量:6

Effects of thoracotomic trauma on the expression of soluble interleukin-2 receptor,interleukin-6 and tumor necrosis factor-α in serum of thoracic tumor patients
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摘要 目的 观察胸部手术创伤对患者血清可溶性白细胞介素 2受体 (SIL 2R)、白细胞介素 6(IL 6)和肿瘤坏死因子 α(TNF α)表达的影响。方法 以患者自身为对照应用酶联免疫吸附法 (ELISA)于麻醉前、手术开始前、施术 2小时及术后 1、3、5天分别检测 2 0例胸部肿瘤患者外周血SIL 2R、IL 6和TNF α的表达。结果 麻醉后SIL 2R、IL 6和TNF α的表达与麻醉前相比均无显著变化 ,施术 2小时各指标均较麻醉前显著降低 :SIL 2R(P <0 .0 1 )、IL 6(P <0 .0 1 )、TNF α(P <0 .0 5) ,术后第一天均达高峰 (SIL 2R :P <0 .0 0 1、IL 6 :P <0 .0 0 1、TNF α :P <0 .0 1 ) ,之后逐渐降低 (术后第 3天 :SIL 2R :P <0 .0 1、IL 6 :P <0 .1、TNF α:P <0 .0 5) ,术后第 5天接近术前水平。结论 外周血SIL 2R、IL 6及TNF α动态变化反映了手术创伤对机体免疫状况的抑制程度 。 Objective To study the effects of thoracotomic trauma on the expression of soluble interleukin 2 receptor (SIL 2R),interleukin 6(IL 6) and tumor necrosis factor α (TNF α) in serum of thoracic tumor patients.Methods ELISA was used to measure parameters in 20 cases.Blood samples were withdrawn from vein before anesthesia,before incision,2 hours of thoracotomy,and 1,3,5 days after operation respectively.Results The levels of SIL 2R,IL 6 and TNF α didn′t change remarkably before incision versus before anesthesia.2 hours of thoracotomy,the value of SIL 2R,IL 6 and TNF α decreased markedly compared with those before anesthesia respectively:P<0.01,P<0.01 and P<0.05.Peak levels appeared on 1st day after operation(SIL 2R:P<0.001;IL 6:P<0.001;TNF α:P<0.01).After then,the value of expression reduced gradually(SIL 2R:P<0.01;IL 6:P<0.1;TNF α:P<0.05 at 3 day after operation).The values of them were closed to levels prior to operation at 5 day after operation.Conclusion The dynamic changes reflect certain suppression of immune status by operative trauma.It is suggested that some measures should be taken for improving patients′ immune function after operation.
出处 《中国肿瘤临床与康复》 2002年第4期10-12,共3页 Chinese Journal of Clinical Oncology and Rehabilitation
关键词 外科手术 可溶性白细胞介素-2受体 白细胞介素-6 肿瘤坏死因子 手术创伤 胸部肿瘤 surgery soluble interleukin 2 receptor interleukin 6 tumor necrosis factor α
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