阿司匹林对急性肺栓塞大鼠肺组织CX3CL1及CX3CR1影响

Effects of aspirin on CX3CL1 and CX3CR1 in acute pulmonary embolism rats

目的探索急性肺栓塞（APE）大鼠不规则趋化因子（CX3CL1）及受体（CX3CRl）的变化及阿司匹林干预作用。方法采用自体血栓法复制APE动物模型，64只大鼠随机分4组：正常组、假手术组、模型组、阿司匹林组。栓塞后4h及72h检测肺病理，肺组织CX3CL1及CX3CRl的免疫组化。结果栓塞72h大鼠肺HE染色呈肺泡壁血管高度扩张、充血，个别大鼠光镜下查见出血性梗死灶，应用阿司匹林后肺组织充血程度明显减轻，出现梗死的大鼠数量也有降低的趋势。CX3CL1主要在胞质和胞膜中表达，CX3CRl主要在胞质和核膜中表达，两者在模型组重度阳性表达（＋＋＋＋），阿司匹林轻微阳性表达（＋），栓塞后4h及72h，正常组、假手术组、阿司匹林组的CX3CL1阳性细胞计数均显著小于模型组（P〈0．05）；栓塞后72h，正常组、假手术组、阿司匹林组的CX3CRl阳性细胞计数均显著小于模型组（10．5±3．5、11．7±5．0、14．6±6．0比20．3±5．4，P〈0．05）。结论阿司匹林能改善APE大鼠的肺部病理，并抑制APE大鼠肺CX3CL1及CX3CRl的表达。

Objective To explore the intervention of aspirin and the changes of CX3CL1 and its receptor CX3CR1 in a rat model of acute pulmonary embolism （APE）. Methods The autologous blood clot method was employed to establish the animal model of APE. A total of 64 rats were randomly divided into 4 groups： normal group （control） , sham operation group （sham）, model group （model） and aspirin group （aspirin）. The profiles of pathology and tissue immunohistochemistry of CX3CL1 and CX3CR1 were compared at 4 h versus 72 h post-embolization. Results At 4 h and 72 h post-embolism, hematoxylin and eosin staining of lung tissue showed a high degree of expansion of alveolar wall vessels and congestion. Furthermore, several rats had hemorrhagic infarction under light microscope. After the dosing of aspirin, hyperemia of lung tissue and the number of rats with infarction significantly decreased. Immunohistoehemistry： CX3CL1 was predominantly expressed in cytoplasm and membrane while CX3CR1 in cytoplasm and nuclear membrane. Both showed strongly positive expression in the model group （ ＋ ＋ ＋ ＋ ） and slightly positive expression in the aspirin group （ ＋ ）. At 4 h and 72 h post-embolization, the CX3CL1 and CX3CRl-positive cell counts of the control, sham and aspirin groups were significantly less than those of the model group （ P 〈 0. 05 ）. Conclusion Aspirin may improve the pathology and inhibit the expression of CX3CL1 and CX3CR1 in APE lung.