To explore the intervention of aspirin and the changes of CX3CL1 and its receptor CX3CR1 in a rat model of acute pulmonary embolism (APE).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.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. Immunohistochemistry: 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 CX3CR1-positive cell counts of the control, sham and aspirin groups were significantly less than those of the model group (P0.05).Aspirin may improve the pathology and inhibit the expression of CX3CL1 and CX3CR1 in APE lung.
