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目的探讨海水淹溺型急性肺损伤时NF-κB活性及TNF-α、IL-1β、IL-10等细胞因子表达量的改变以及地塞米松对其可能的影响。方法42只新西兰兔随机分成对照组(n=18)、模型组(n=12)和地塞米松治疗组(n=12)。模型组经气管插管灌注2ml/kg海水造成海水淹溺型急性肺损伤,地塞米松治疗组在造模同时经颈总动脉插管给予地塞米松1mg/kg。观察各组动物血气分析的动态变化,计算肺湿干质量比(W/D)、肺通透指数(LPI)。以非放射性凝胶迁移实验分析肺组织NF-κB活性,ELISA法检测肺组织TNF-α、IL-1β、IL-10浓度。H-E染色进行病理学检查,并计算肺病理评分(LPS)。结果与对照组比,模型组兔肺大体标本淤血水肿严重,体积明显增大,显微镜下可见炎性细胞浸润等急性肺损伤病理学征象;氧合指数迅速低至300mmHg(1mmHg=0.133kPa)以下,持续时间长达6h;W/D于海水灌注后3h达高峰,肺通透指数及肺病理评分以海水灌注后6h数值最高;肺组织NF-κB活性及TNF-α、IL-1β、IL-10等细胞因子表达量明显增高(P<0.05,P<0.01)。地塞米松治疗组病理学改变比对照组重,但比模型组轻;W/D、肺通透指数及肺病理评分也都比模型组低;氧合指数在海水灌注后6h亦得到明显改善;NF-κB活性及TNF-α、IL-1β、IL-10浓度均显著低于模型组(P<0.05,P<0.01)。结论地塞米松可抑制海水淹溺型急性肺损伤时肺组织NF-κB活性及TNF-α、IL-1β、IL-10等细胞因子的表达,减轻肺组织的炎症反应和病理损害。
Objective To investigate the changes of NF-κB and TNF-α, IL-1β, IL-10 and other cytokines in seawater drowning acute lung injury and the possible effect of dexamethasone. Methods Forty-two New Zealand white rabbits were randomly divided into control group (n = 18), model group (n = 12) and dexamethasone treatment group (n = 12). The rats in the model group were infused with 2ml / kg seawater via tracheal intubation to induce seawater drowning-type acute lung injury. Dexamethasone treatment group was given dexamethasone 1mg / kg through the common carotid artery while modeling. The dynamic changes of blood gas analysis in each group were observed and the wet / dry weight ratio (W / D) and pulmonary permeability index (LPI) were calculated. The activity of NF-κB in lung tissue was analyzed by non-radioactive gel migration assay. The concentrations of TNF-α, IL-1β and IL-10 in lung tissue were detected by ELISA. H-E staining pathological examination, and calculate the lung pathological score (LPS). Results Compared with the control group, the congestion and edema in the lung tissue of the model group were severe and the volume was significantly increased. The pathological signs of acute lung injury such as inflammatory cell infiltration were observed under the microscope. The oxygenation index rapidly dropped below 300mmHg (1mmHg = 0.133kPa) , The duration of up to 6h; W / D peaked at 3h after seawater perfusion, pulmonary permeability index and lung pathology score 6h after seawater perfusion, the highest value; lung tissue NF-κB activity and TNF-α, IL-1β, IL -10 and other cytokines were significantly increased (P <0.05, P <0.01). Dexamethasone treatment group pathological changes heavier than the control group, but lighter than the model group; W / D, pulmonary permeability index and lung pathological score are also lower than the model group; oxygenation index 6h after seawater was also significantly improved ; NF-κB activity and TNF-α, IL-1β and IL-10 concentrations were significantly lower than the model group (P <0.05, P <0.01). Conclusion Dexamethasone can inhibit the expression of NF-κB and TNF-α, IL-1β, IL-10 and other cytokines in lung tissue of acute lung injury in seawater drowning, and reduce the inflammatory reaction and pathological damage in lung tissue.