Objective To explore the intervention of aspirin on tumor necrosis factor alpha (TNF-α) of rats with acute pulmonary (APE). Methods A total of 64 rats were randomly divided into 4 groups which were normal group(control), sham operation group(sham), model group(model) and aspirin group(aspirin) with 16 rats in each. The autologous blood clot were token to copy the APE animal mode. The serum TNF-αand the mRNA expression level of lung tissue were com-pared at 4-hour versus 72-hour after modeling. Results At 4-hour and 72-hour post-embolization, the control group and sham group showed normal lung tissue, the lung tissue of model group was significantly associated with alveolar wall con-gestion, emphysema, mild edema and inflammatory cells infiltration. At 4-hour after modeling, the degree of lung tissue lesion in the aspirin group was lighter than in the model group, the main lesions was alveolar wall edema while at 72-hour after modeling, the main pathological changes in lung tissue was mild or moderate hyperemia of alveolar walls, edema and inflammatory cell infiltration. The serum TNF-αamong four groups were significantly different at 4-hour and 72-hour after modeling (F=6.59, 23.09, P<0.05). The further multiple comparison showed that the level of serum TNF-α in aspirin group was significantly higher than those in the control group, sham group and model group at 4-hour after modeling (t=4.38,2.67,2.90,P<0.05). The levels of serum TNF-α in model was significantly higher than the control group, sham group and aspirin group at 72-hour af-ter modeling(t=5.43,7.37,6.64,P<0.05). The TNF-αmRNA among four groups were significantly differ-ent at 4-hour and 72-hour after modeling (F=39.35, 72.05,P<0.05). The TNF-α mRNA expression in lung tissue of the model group were significantly higher than those in control group, sham group and aspirin group at 4- hour and 72-hour after modeling(t=9.72, 8.36, 8.24; 12.12, 12.04, 11.85, P<0.05). Conclusion Aspirin can play an inhibitory effect on TNF-α in pulmonary embolism after 72 hours and has a protective effect on acute pulmonary embolism.%目的：探索阿司匹林对急性肺栓塞（APE）大鼠肿瘤坏死因子-α（TNF-α）的干预作用。方法64只大鼠随机分为4组，每组16只：正常组、假手术组、模型组、阿司匹林组。采用自体血栓法复制APE动物模型，比较四组造模后4 h、72 h的血清TNF-α及肺组织TNF-α的mRNA表达水平。结果病理见造模4 h及72 h后，对照组及假手术组呈正常肺组织结构，模型组肺组织主要为肺泡壁明显充血，伴有肺气肿、轻度水肿和炎细胞浸润，阿司匹林组造模后4 h，肺组织病变程度较模型组轻，主要病变为肺泡壁水肿，造模后72 h，肺组织主要病变为肺泡壁轻度或中度充血、水肿、炎细胞浸润。四组造模后4 h、72 h血清TNF-α水平比较，差异均有统计学意义（F分别＝6.59、23.09， P均＜0.05）。进一步两两比较发现，造模后4 h，阿司匹林组血清TNF-α水平明显高于对照组、假手术组、模型组（t分别＝4.38、2.67、2.90，P均＜0.05）。造模后72 h，模型组血清TNF-α水平明显高于对照组、假手术组和阿司匹林组，差异有统计学意义（t分别＝5.43、7.37、6.64，P均＜0.05）。四组造模后4 h、72 h肺组织TNF-α的mRNA表达水平比较，差异均有统计学意义（F分别＝39.35、72.05，P均＜0.05）。进一步两两比较发现，模型组造模后4 h、72 h肺组织TNF-α的mRNA表达水平均明显高于对照组、假手术组、阿司匹林组（t分别＝9.72、8.36、8.24；12.12、12.04、11.85，P均＜0.05）。结论阿司匹林在72 h后才能发挥对肺栓塞TNF-α的抑制作用，对APE起一定的保护作用。
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