一氧化碳中毒及迟发性脑病与血清中免疫相关细胞因子的表达

Carbon monoxide poisoning and delayed encephalopathy associated with expres- sion of immune related cytokines in serum

目的:检测一氧化碳中毒后迟发性脑病(DEACMP)患者血清中IL-4、IL-10、IFN-γ、TGF-β1的水平,探讨DEACMP与神经免疫的相关性。方法:实验分为一氧化碳中毒后迟发性脑病组(DEACMP组)、急性一氧化碳中毒未发生迟发性脑病组(ACOP组)及健康对照组。应用酶联免疫吸附法(ELISA)测定30例DEACMP患者、27例ACOP患者及28例健康对照者中血清IL-4、IL-10、IFN-γ、TGF-β1水平,运用相关统计方法分析比较各组数值的差异。结果:DEACMP组IL-4水平低于健康对照组(P<0.05),ACOP组低于健康对照组(P<0.05);DEACMP组IL-10水平低于ACOP组(P<0.05),ACOP组高于健康对照组(P<0.05);DEACMP组IFN-γ水平高于ACOP组及健康对照组(P<0.05),ACOP组高于健康对照组(P<0.05);DEACMP组TGF-β1水平低于ACOP组及健康对照组(P<0.05),ACOP组高于健康对照组(P<0.05)。结论:一氧化碳中毒后迟发性脑病的发生与神经免疫损伤机制有关。

Objective：To detect the levels of the IL-4, IL-10, IFN-γ, TGF-β1 in the serum with the patient＇ s condition of delayed eneephalopathy after carbon monoxide poisoning（DEACMP）. To explore the relationship between DEACMP and neuroimmunological correlation. Methods： Experiments were divided into three groups： delayed encephalopathy after carbon monoxide poisoning group （ DEACMP）, acute carbon monoxide poisoning without delayed encephalopathy group （ACOP） and healthy control group. Using methods of enzyme-linked immuno-sorbent assay （ELISA）, we determined the serum levels of IL-4 ,IL-10 ,TGF-β1 and IFN-3, from 30 patients with DEACMP, 27 patients with ACOP and 28 with healthy control. Using statistical analysis compared the difference between three groups. Results： The level of IL-4 in DEACMP was lower than the healthy control group （ P 〈 O. 05 ） ; ACOP group was lower than the healthy control group （ P 〈 0.05 ） ; the level of IL-10 in DEACMP was lower than the ACOP group （ P 〈 0.05 ）, the ACOP group was higher than the healthy control group （ P 〈 0.05 ） ; IFN-γ level in the blood of DEACMP group was higher than that of ACOP group and healthy control group （P 〈 0. 05 ） ; ACOP group was higher than the healthy control group （P 〈 0. 05 ） ; TGF-β1 in DEAC- MP group blood level was below the ACOP group and healthy control group （ P 〈 0.05 ） ; ACOP group was higher than the healthy control group （P 〈 0.05 ） . Conclusion： The occurrence of delayed eneephalopathy after carbon monoxide poisoning is associated with neural immune mechanism of injury.