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Macrophage Depletion by Clodronate Liposomes Suppresses Neointimal Formation After Carotid Artery Injury in Apolipoprotein E-Deficient Mice

Macrophage Depletion by Clodronate Liposomes Suppresses Neointimal Formation After Carotid Artery Injury in Apolipoprotein E-Deficient Mice

초록/요약

Background and Objectives : Clodronate liposomes deplete phagocytic cels, thereby suppresing inflammation after vascular injury. We compared the efect of clodronate liposomes on macrophage depletion and neointimal formation in apolipoprotein E-deficient mice [ApoE (-) mice]. Materials and Methods : ApoE (-)to the clodronate liposomes group (Clodronate Group, n=7) and the vehicle liposomes group (Control Group, n=7). Clodronate (0.1 mL/10 g) was injected via the tail vein starting 2 days (d-2) before left common carotid artery injury. Results: The percentage of blod monocytes was subsequently decreased after clodronate injection (14.0± 7.4% at baseline, 6.8± 4.9% at 24 hours and 0.7± 0.3% at 1 wek after the clodronate liposome injection). The percentage of macrophages in the plaque area was significantly lower in the clodronate group at week 2 (32.0± 6.5 vs. 68.7±7.6%, respectively, p<0.05) and at wek 4 (37.3± 8.5 vs. 62.6± 9.4%, respectively, p<0.05). The interleukin (IL)-6 and tumor necrosis factor (TNF)-α concentrations were significantly decreased in the clodronate group at wek 4 (12.3± 2.5 vs. 22.9± 3.5 pg/mL, respectively, p<0.05 for IL-6 and 16.6± 2.2 vs. 43.6± 6.1 pg/mL, respectively, p<0.05 for TNF-α). The plaque volume was significantly greater in the control group at week 2 (0.345± 0.063 vs. 0.153± 0.053 mm2, respectively, p<0.05) and at week 4 (0.320± 0.027 vs. 0.167± 0.070 mm2, respectively, p<0.05). Conclusion : Intravenous administration of clodronate liposomes depleted monocytes and macrophages, and so this reduced the inflammatory markers and neointimal formation in ApoE (-) mice.

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