Abstract:

BACKGROUND: Restenosis after angioplasty frequently occurs. Inflammatory response is the initiating factor of restenosis. Therefore, to effectively suppress inflammation and reduce smooth muscle cell migration and proliferation is the key to reducing restenosis. Studies have demonstrated that cilostazol significantly reduces restenosis after angioplasty, but the mechanism remains unclear.
OBJECTIVE: To investigate the efficacy and mechanism of the cilostazol treatment of rabbit iliac artery restenosis.
METHODS: The white rabbits were randomly divided into 6 groups (blank control, vascular stenosis, vascular restenosis, cilostazol 25, 50 and 100 mg/kg groups), and fed with high fat food. Iliac artery stenosis model was established in all groups except blank control group. Percutaneous transluminal angioplasty was performed at stenosis site of vascular restenosis and cilostazol groups. Angiography was performed to determine blood lipid and cytokine mass concentration. Nuclear factor-κB expression was observed by immunohistochemistry, and vascular stenosis was analyzed using imaging work station.
RESULTS AND CONCLUSION: Compared with the restenosis group, the blood lipids and cytokines concentration was significantly decreased following cilostazol treatment (P < 0.05). Immunohistochemistry showed that the nuclear factor-κB expression in restenosis group was significantly greater than the blank control and cilostazol groups, but the expression was decreased with increasing cilostazol dose (P < 0.05). Angiography confirmed that vessel area stenosis rate and rates of diameter stenosis were significantly decreased in cilostazol group compared with the restenosis group (P < 0.01). Results showed that cilostazol can inhibit the rabbit iliac artery restenosis, possibly by regulating nuclear factor-κB and inhibiting various inflammatory factors.