芬太尼对人外周血NF-κB活性的影响

目的　验证芬太尼是否影响免疫炎症反应中的某些因素 ,如同吗啡。方法　外周血取自 7个正常志愿者 ,实验分为正常对照组、芬太尼 ( 2 0 μg·L-1和 2mg·L-1)组、模型组(脂多糖 ,LPS组 )和治疗组 (芬太尼 2 0 μg·L-1+LPS、芬太尼 2mg·L-1+LPS)。用流式细胞术检测人外周血中性粒细胞和单核细胞中核因子(NF κB)活性 ,用ELISA检测血清中肿瘤坏死因子 α(TNF α)和白介素 6(IL 6)含量。结果　芬太尼组NF κB活性及TNF α和IL 6含量与正常对照组比较 ,均无明显差异 (P >0 .0 5 )。治疗组 (芬太尼 2 0 μg·L-1+LPS、芬太尼 2mg·L-1+LPS)中NF κB的活性分别为 81 .9% ,76.1 % (中性粒细胞 )和 78.6% ,72 .6%(单核细胞) ,明显低于模型组 88.9%和 85 .1 % (P <0 .0 1 )。TNF α含量在治疗组 (芬太尼 2 0 μg·L-1+LPS、芬太尼 2mg·L-1+LPS)为 45 9和 3 5 7ng·L-1,IL 6为 796和 72 0ng·L-1,两者均低于模型组 (其中TNF α为 1 2 2 6ng·L-1,IL 6为 1 5 63ng·L-1) (P <0 .0 1 )。结论　芬太尼对NF κB的活性及TNF α和IL 6的含量无影响 ,但可抑制LPS诱导的NF κB的活性及TNF α和IL 6的含量 ,且高剂量芬太尼的抑制作用大于低剂量芬太尼的作用

Effects of fentanyl on activation nuclear factor-kappaB in human whole blood

AIM To clarify if fentanyl affects some factors in immunity and inflammation as morphine did. METHODS Blood samples were collected from 7 healthy volunteers. Each was divided into 6 parts: normal control, fentanyl(20 μg·L^-1 or 2 mg·L^-1) control, lipopolysaccharide(LPS) alone and fentanyl 20 μg·L^-1 or 2 mg·L^-1+LPS. The nuclear factor- kappaB(NF-κB) activation in human neutrophils and monocytes was examined by flow cytometric analysis, the plasma tumor necrosis factorα(TNF-α) and interleukin-6(IL-6) concentrations were measured using ELISA. RESULTS The low NF- κB activation (2.8%－4.0%) and TNF-α and IL- 6 production was no significant difference in normal control and fentanyl control(P>0.05). The NF-κB activation in treatment groups(fentanyl 20 μg·L^-1+LPS, fentanyl 2 mg·L^-1+LPS) were 81.9% and 76.1% in neutrophils and 78.6% and 72.6% in monocytes, respectively, which were less than those in LPS alone group（88.9% and 85.1%, P<0.01). TNF-α production in treatment groups(fentanyl 20 μg·L^-1+LPS, fentanyl 2 mg·L^-1+LPS) and LPS group were 459, 357 and 1226 ng·L^-1, IL- 6 were 796, 720 and 1563 ng·L^-1, respectively. The differences were significant between treatment groups and LPS one(P<0.01). CONCLUSION Fentanyl alone has no effect on NF- κB activation and TNF-α and IL-6 production, but attenuates LPS-induced NF- κB activation and TNF-α and IL-6 production.