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目的探索建立输血相关急性肺损伤(TRALI)小鼠模型。方法雄性Balb/c小鼠随机分为5组(分别命名为A、B、C、D及E组),前4组小鼠5只/组,E组15只/组。E组(TRALI模型组):每只小鼠腹腔注射1 mg/m L脂多糖(LPS)预处理,注射剂量为0.1 mg/(kg·只),24 h后尾静脉注射1 mg/m L H2Kd单克隆抗体,注射剂量为2.25mg/(kg·只),建立TRALI小鼠模型;其余均为对照组,其中A为空白对照组,B为注射LPS组,C为注射LPS及24 h后注射生理盐水(NS)组,D为注射H2Kd单克隆抗体组。分析各组小鼠肺组织病理、肺湿重/干重比、直肠温度、死亡率等指标,建立TRALI小鼠模型,并以此为基础,对阿司匹林(ASA)干预小鼠TRALI的效果做验证。结果与对照组相比,TRALI模型组小鼠2 h的直肠温度(31.060±0.472)℃,明显低于其他各对照组小鼠(P<0.01),肺湿重/干重比为7.642±1.309,则较其他各组明显增加(P<0.01);TRALI模型组小鼠肺组织出现肺泡间隔增厚,肺泡壁断裂,肺泡内纤维蛋白浸润等病理变化,符合TRALI急性肺损伤典型的症状及体征;在ASA干预后2 h,TRALI小鼠死亡率为0,肺水肿明显减轻(P<0.01)。结论成功建立了TRALI小鼠模型,该模型能够模拟TRALI的临床表现,可重复性强,稳定性好,有助于解释TRALI病理过程、探索TRALI的救治措施。
Objective To establish a mouse model of transfusion-related acute lung injury (TRALI). Methods Male Balb / c mice were randomly divided into 5 groups (named as A, B, C, D and E, respectively), 5 mice in the first 4 groups and 15 mice in the E group. Group E (TRALI model group): Each mouse was pretreated with LPS (1 mg / m L) by intraperitoneal injection at a dose of 0.1 mg / (kg · kg) H2Kd monoclonal antibody at a dose of 2.25mg / (kg · kg) to establish TRALI mouse model; the rest were control group, A was blank control group, B was injected LPS group, C was LPS injection and 24 h after injection Inject saline (NS) group, D is inject H2Kd monoclonal antibody group. The lung tissue pathology, lung wet weight / dry weight ratio, rectal temperature, mortality and other indicators of mice in each group were analyzed to establish the TRALI mouse model and to verify the effect of aspirin (ASA) on mouse TRALI . Results Compared with the control group, the rectal temperature (31.060 ± 0.472) ℃ for 2 h in TRALI model group was significantly lower than that in other control mice (P <0.01), and the lung wet weight / dry weight ratio was 7.642 ± 1.309 (P <0.01). The pathological changes of alveolar septum thickening, alveolar wall rupture and alveolar fibrin infiltration were observed in the lungs of TRALI model group, which were in line with the typical symptoms and signs of TRALI acute lung injury At 2 h after ASA intervention, the mortality of TRALI mice was 0, and pulmonary edema was significantly reduced (P <0.01). Conclusion The TRALI mouse model was successfully established. This model can simulate the clinical manifestations of TRALI. It has strong repeatability and good stability, which is helpful to explain the pathological process of TRALI and explore the treatment of TRALI.