芬太尼对人外周血NF-κB活性的影响

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

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 。

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.