中国临床药理学与治疗学
中國臨床藥理學與治療學
중국림상약이학여치료학
CHINESE JOURNAL OF CLINICAL PHARMACOLOGY
2003年
2期
155-157
,共3页
药效学%吗啡%肿瘤坏死因子-α%白细胞介素-6
藥效學%嗎啡%腫瘤壞死因子-α%白細胞介素-6
약효학%마배%종류배사인자-α%백세포개소-6
pharmacodynamics%morphine%tumor necrosis factor-α%interleukin-6
目的:研究吗啡对人外周血中肿瘤坏死因子-α (TNF-α)和白细胞介素-6 (IL-6)含量的影响,探讨其对免疫炎症反应的可能机制.方法:全血收集在试管内,分装在EP管中,每管取100 μl全血.实验分为吗啡200 mg*L-1组(A1组)、吗啡2 mg*L-1组(A2组)、吗啡200 mg*L-1+脂多糖(LPS)(B1组)、吗啡2 mg*L-1组+LPS(B2组)、对照组(C1组)和LPS组(C2组)共6组(n=7).各组加入上述试剂,用PBS补齐体积后,在37℃下孵育6 h.用ELISA检测血清中TNF-α和IL-6含量.结果:单独药物组(A1和A2组)TNF-α的浓度分别为240和251 ng*L-1,与空白对照组(C1组,TNF-α的浓度为279 ng*L-1)比较,无显著的统计学意义(P>0.05);IL-6的浓度分别为444、490和561 ng*L-1,亦无统计学意义(P>0.05).激活组(B1和B2组)和LPS组(C2组)分别为490、534和1226 ng*L-1 (TNF-α); 1177、1310和1563 ng*L-1 (IL-6).B1和B2组明显低于C2组(P<0.01或P<0.05),且B1组低于B2组.结论:吗啡对静息状态下TNF-α的表达无影响,但可抑制LPS诱导的TNF-α表达,且高剂量的吗啡对LPS诱导的TNF-α的抑制作用大于低剂量吗啡的作用.
目的:研究嗎啡對人外週血中腫瘤壞死因子-α (TNF-α)和白細胞介素-6 (IL-6)含量的影響,探討其對免疫炎癥反應的可能機製.方法:全血收集在試管內,分裝在EP管中,每管取100 μl全血.實驗分為嗎啡200 mg*L-1組(A1組)、嗎啡2 mg*L-1組(A2組)、嗎啡200 mg*L-1+脂多糖(LPS)(B1組)、嗎啡2 mg*L-1組+LPS(B2組)、對照組(C1組)和LPS組(C2組)共6組(n=7).各組加入上述試劑,用PBS補齊體積後,在37℃下孵育6 h.用ELISA檢測血清中TNF-α和IL-6含量.結果:單獨藥物組(A1和A2組)TNF-α的濃度分彆為240和251 ng*L-1,與空白對照組(C1組,TNF-α的濃度為279 ng*L-1)比較,無顯著的統計學意義(P>0.05);IL-6的濃度分彆為444、490和561 ng*L-1,亦無統計學意義(P>0.05).激活組(B1和B2組)和LPS組(C2組)分彆為490、534和1226 ng*L-1 (TNF-α); 1177、1310和1563 ng*L-1 (IL-6).B1和B2組明顯低于C2組(P<0.01或P<0.05),且B1組低于B2組.結論:嗎啡對靜息狀態下TNF-α的錶達無影響,但可抑製LPS誘導的TNF-α錶達,且高劑量的嗎啡對LPS誘導的TNF-α的抑製作用大于低劑量嗎啡的作用.
목적:연구마배대인외주혈중종류배사인자-α (TNF-α)화백세포개소-6 (IL-6)함량적영향,탐토기대면역염증반응적가능궤제.방법:전혈수집재시관내,분장재EP관중,매관취100 μl전혈.실험분위마배200 mg*L-1조(A1조)、마배2 mg*L-1조(A2조)、마배200 mg*L-1+지다당(LPS)(B1조)、마배2 mg*L-1조+LPS(B2조)、대조조(C1조)화LPS조(C2조)공6조(n=7).각조가입상술시제,용PBS보제체적후,재37℃하부육6 h.용ELISA검측혈청중TNF-α화IL-6함량.결과:단독약물조(A1화A2조)TNF-α적농도분별위240화251 ng*L-1,여공백대조조(C1조,TNF-α적농도위279 ng*L-1)비교,무현저적통계학의의(P>0.05);IL-6적농도분별위444、490화561 ng*L-1,역무통계학의의(P>0.05).격활조(B1화B2조)화LPS조(C2조)분별위490、534화1226 ng*L-1 (TNF-α); 1177、1310화1563 ng*L-1 (IL-6).B1화B2조명현저우C2조(P<0.01혹P<0.05),차B1조저우B2조.결론:마배대정식상태하TNF-α적표체무영향,단가억제LPS유도적TNF-α표체,차고제량적마배대LPS유도적TNF-α적억제작용대우저제량마배적작용.
AIM:To study the effects of morphine on tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) production in human whole blood and the possible mechanism. METHODS: The seven human whole blood samples were collected, and each was aliquoted in six tubes. A total of 100 μl of whole blood was added with morphine sulfate (200 mg*L-1 and 2 mg*L-1). Then lipopolysaccharide (LPS) (100 μg*L-1) was added to the blood and incubated for 6 h at 37 ℃. Each whole blood was divided into six groups: drug-alone groups (groupA1, morphine 200 mg*L-1; group A2, morphine 2 mg*L-1), activation groups (group B1, morphine 200 mg*L-1+LPS; group B2, morphine 2 mg*L-1+LPS), control group (group C1), and LPS group (group C2). The concentrations of TNF-α and IL-6 in plasma were measured by ELISA. RESULTS: The values of TNF-α production in group A1, A2 and C1 were 240, 251, and 279 ng*L-1 (P>0.05), respectively; the values of IL-6 were 444, 490, and 561 ng*L-1 (P>0.05), respectively. The cytokine production in groupB1, B2 and C2 were 490, 534 and 1226 ng*L-1 (TNF-α), respectively; 1177, 1310 and 1563 ng*L-1 (IL-6), respectively. The levels in group B1 and B2 were less than that in group C2 (P<0.01, or P<0.05), and the level in B1 was less than that in B2. CONCLUSION: Morphine alone has no effects on TNF-α and IL-6 production, but attenuates LPS-induced TNF-α and IL-6 production, and the high dose of morphine-induced effects on attenuation of TNF-α and IL-6 production increased are more than the low dose.
