Abstract: Objective · To investigate the effect of albendazole (ABZ) on mouse femoral arteries restenosis and explore its possible mechanism. Methods · Vascular smooth muscle cells (VSMCs) were cultured in vitro with 0.5 and 1 μmol/L ABZ, and evaluated for cell proliferation, migration, and apoptosis by MTT, Transwell assay, and Annexin V-PI staining flow cytometry, respectively; and Western blotting was also used for the analysis of phosphorylation mechanism of cytoskeleton proteins cofilin (CFL) and myosin light chain (MLC). Stenosis was established in the unilateral femoral artery of 10-week-old wildtype male C57BL/6 mice by perivascular cuff placement and high fat chow breeding for 4 weeks. After successful modeling, mice were randomly divided into control group (equal volume of solvent) and ABZ group (1.5 mg/d) for gavage, and femoral arteries were collected 4 weeks later for H-E histological analysis of intimal area, medial area, and intima/media (I/M) ratio to clarify the severity of restenosis. Results · Both 0.5 and 1 μmol/L ABZ could significantly inhibit the proliferation and migration of VSMCs (both P<0.05), while 0.5 μmol/L had no significant effect on the apoptosis of VSMCs. ABZ gavage could significantly reduce the neointimal area and I/M ratio in the restenosis mice, while there were no effects on the median area. Both 0.5 and 1 μmol/L ABZ treatment could significantly inhibit CFL dephosphorylation and MLC phosphorylation, which showed a concentration-dependent trend (both P<0.05). Conclusion · ABZ inhibits VSMCs migration and intimal hyperplasia, via affecting the phosphorylation of cytoskeleton protein CFL and MLC, thereby resulting in therapeutic effects on restenosis of mice.

Key words: albendazole, vascular smooth muscle cell, intimal hyperplasia, vascular occlusion, mechanism