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目的 观察肿瘤坏死因子 α (TNF α)和白介素 - 1 0 (IL - 1 0 )在大鼠一氧化碳 (carbonmonoxide,CO)中毒后不同时点脑内的表达 ,探讨它们在CO中毒脑损伤中的作用。方法 建立大鼠急性CO中毒模型 ,用双抗体夹心ELISA法检测大鼠CO中毒后不同时点脑组织匀浆中TNF α与IL - 1 0的水平。结果 大鼠CO中毒后 3h脑TNF α水平升高 (P <0 0 5) ,6h达高峰 (P <0 0 1 ) ,2 4h仍高水平表达 (P <0 0 1 ) ,至 72hTNF α水平有所下降 ,但仍高于对照组 (P <0 0 5) ;脑IL - 1 0水平于中毒后 2 4h开始升高达峰值 (P <0 0 5) ,至 72h有所下降 ,但仍高于对照组 (P <0 0 5)。结论 脑内TNF α在CO中毒后迅速表达并持续升高 ,可能作为损伤介质参与了CO中毒脑损伤的发生 ,IL - 1 0水平升高较TNF α延迟出现 ,可能在急性CO中毒晚期发挥神经元保护作用
Objective To observe the expression of tumor necrosis factor α (TNF α) and interleukin 10 (IL - 10) in the brain at different time points after carbon monoxide (CO) intoxication in rats, and to explore their roles in brain injury induced by carbon monoxide . Methods The model of acute CO poisoning in rats was established. The levels of TNFα and IL - 1 0 in brain homogenate of rats at different time points after CO poisoning were determined by double antibody sandwich ELISA. Results The level of TNFα increased 3h after CO poisoning in rats (P <0 05), peaked at 6h (P 0 01) and remained high at 24 h (P 0 01) (P <0.05). The level of IL - 10 in brain increased from the 24th hour after poisoning to the peak (P <0 05), but decreased to the level of 72 hours, but remained high In the control group (P <0 05). Conclusions TNFα in brain is rapidly expressed and persistently increased after CO poisoning. It may play a role as a damaging mediator in the pathogenesis of CO poisoning and brain injury. Elevated IL - 10 level appears later than that of TNFα and may play a role in the later stage of acute CO poisoning Yuan protection role