吗啡和芬太尼对人外周血肿瘤坏死因子-α和白细胞介素-6表达的影响

目的 :研究吗啡和芬太尼对人外周血肿瘤坏死因子 α(TNF α)和白细胞介素 6(IL 6)表达的影响并探讨其机制。方法 :试验分单独药物组 (A1:吗啡 2 0 0mg·L-1,A2 :吗啡 2mg·L-1,A3 :芬太尼 2mg·L-1和A4:芬太尼 2 0 μg·L-1)、激活组〔A1,A2 ,A3 和A4组加入脂多糖 (LPS) ,称为B1,B2 ,B3 和B4组〕和对照组 (C1:空白对照和C2 :LPS对照 ) ,共 1 0组。检测 7份正常人血标本。用ELISA检测TNF α和IL 6含量。结果 :A组TNF α浓度为 1 84～2 5 1ng·L-1;IL 6为 3 96～ 490ng·L-1。与C1组 (TNF α:2 79ng·L-1;IL 6:5 61ng·L-1)比较 ,差异无显著意义 (P >0 .0 5 )。B组TNF α浓度为 3 5 7～5 3 4ng·L-1;IL 6为 72 0～ 1 3 1 0ng·L-1,明显低于C2 组(TNF α:1 2 2 6ng·L-1;IL 6:1 5 63ng·L-1) (P <0 .0 5 ;P <0 .0 1 ) ,且高剂量组低于其低剂量组。结论 :吗啡和芬太尼不影响静息状态下TNF α和IL 6的表达 ,但可抑制LPS诱导的TNF α和IL 6表达 ,且具有明显量效关系

Effects of morphine and fentanyl on tumor necrosis factor-α and interleukin-6 expression in human peripheral blood

AIM: To study the effects of morphine and fentanyl on tumor necrosis factor- α(TNF-α) and interleukin-6(IL-6) expression in human peripheral blood and t he possible mechanisms. METHODS: Each sample of peripheral blood collected from 7 healthy men was divid ed into ten groups:Drug-alone groups (gropu A 1:morphine 200 mg·L -1 ,gr oup A 2: morphine 2 mg·L -1 ,group A 3: fentanyl 2 mg·L -1 , group A 4: fentanyl 20 μg·L -1 );Activation groups were named group B 1,B 2,B 3,an d B 4 in which lipopolysaccharide (LPS 100 μg·L -1 ) was added into their corresponding group A 1-A 4; and control group(group C 1:blank, and group C 2:LPS 100 μg·L -1 ).The plasma TNF-α and IL-6 concentrations were mea sured by using ELISA assay. RESULTS: Cytokines expression in groups A was 184-251 ng·L -1 (TNF -α); 396-490 ng·L -1 (IL-6).There was no significant difference compar ed with group C 1(TNF-α:279 ng·L -1 ; IL-6:561 ng·L -1 )(P> 0. 05 ).The expression in groups B was 357-534 ng·L -1 (TNF-α); 720-1 3 10 ng·L -1 (IL-6), the levels in groups B were lower than those in group C 2( TNF-α:1 226 ng·L -1 ; IL-6:1 563 ng·L -1 )(P<0.05,P<0.01),and th e high-dose morphine and fentanyl groups (group B 1 and B 3) were lower than those in their low-dose(group B 2 and B 4). CONCLUSION:Morphine and fentanyl have no significant effect on the TNF-α and IL-6 levels of peripheral blood , but both attenuate LPS-induced TNF-α and IL-6 expression in dose-dependen t manner.