The present study aimed to explore the influence of
aspirin on the CX3CL1/CX3CR1 signaling pathway in acute
pulmonary embolism (APE) in rats. Our previous study found that CX3CL1/CX3CR1 was increased in APE. However, the effect of this signaling pathway on APE remains unclear. CX3CL1-shRNA adenovirus and CX3CL1-overexpression vector were constructed. Male Sprague-Dawley rats were randomly divided into 9 groups (n=10): normal group (group N),
sham operation group (group Sham),
sham operation +
aspirin group (group ASP), model group (group M), model + ASP group (group M+A), model +
shRNA group (group M+SH),
sham operation + CX3CL1-overexpression vector group (group Sham+Cx3), model + ASP +
shRNA group (group M+A+SH), and model + ASP + CX3CL1-overexpression vector group (group M+A+CX3). Arterial pressure detection,
hematoxylin and
eosin staining, reverse transcription-polymerase chain reaction,
enzyme-linked
immunosorbent assay, and
laser confocal scanning microscopy were applied.
Aspirin significantly decreased pulmonary artery pressure, improve pathological changes in the
embolism, and decreased the expression of CX3CL1/CX3CR1 and CX3CL1/NF-κB. Moreover, the adenovirus-overexpression CX3CL1 vector aggravated the inflammatory changes in APE, which were improved by
aspirin. However, the intervention of the adenovirus CX3CL1 vector reduced the change, while its combination with
aspirin significantly improved the change. In conclusion,
aspirin improved pathological changes in rats with APE via the CX3CL1/CX3CR1 signaling pathway.