Synthetic E-selectin prevents postoperative vascular restenosis by inhibiting nuclear factor κB in rats.

During the development of postoperative vascular restenosis, the aberrant proliferation of vascular smooth muscle cells (VSMCs) is a critical event resulting in intimal hyperplasia. Inflammatory responses involving the activation of nuclear factor (NF)‑κB are among the major molecular processes underlying restenosis. The present study aimed to investigate the roles of NF‑κB in VSMC proliferation and restenosis following vascular anastomosis, as well as to evaluate the potential of synthetic E‑selectin to downregulate NF‑κB and thus inhibit vascular hyperplasia. A total of 72 adult male Sprague‑Dawley rats were randomly assigned to three groups: Control, operation and treatment groups. Rats in the operation and treatment groups received longitudinal incisions in the right carotid arteries, which were closed using interrupted sutures. Following vascular anastomosis, synthetic E‑selectin (10 mg/kg), or an equal volume of saline, was immediately injected into the right femoral vein of rats in the treatment and operation groups, respectively. Following surgery, the mRNA and protein expression levels of NF‑κB at the site of anastomosis, the levels of tumor necrosis factor‑α and interleukin‑6 in the serum, NF‑κB binding activity, and the presence of proliferating cell nuclear antigen (PCNA)‑positive cells were evaluated by western blotting, reverse transcription‑quantitative polymerase chain reaction, ELISA, electrophoretic mobility shift assay and immunofluorescence staining. The present results demonstrated that following treatment with synthetic E‑selectin, the levels of NF‑κB and the inflammatory response, as well as the presence of PCNA‑positive cells, were significantly reduced (P<0.01). In conclusion, the results of the present study suggested that synthetic E‑selectin may exert anti‑inflammatory and anti‑restenotic effects following vascular anastomosis in vivo.