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In recent years, various adhesion molecules have been discovered. Very late antigen-4 (VLA-4), an adhesion molecule belonging to the integrin family, plays an important role in lymphocyte migration and infiltration into sites of in ammation. In the present study, we investigated whether administration of antiVLA-4 monoclonal antibody (mAb) reduces in ammation in ischemia-reperfusion injury using a skin flap model in Sprague-Dawley rats. A superficial epigastric arteriovenous pedicle ap, sized 45×30 mm, was elevated in the right inguinal area. The vessel was clamped to induce ischemia and the clamp was removed after 9 hours. Fifteen minutes prior to clamp release, the rats were administered antiVLA-4 mAb (0.2 mg / kg i.v., n= 10) or saline (n= 10). At the same time, a sham group (n= 5) was established with a similar operation but the vessel was only clamped to induce ischemia for 5 minutes. Anti-VLA-4 mAb significantly improved the survival area of the skin ap to 92.4% (median), when compared to 12.5% (median) in the control group. Severe in ammatory cell in ltration and edema was consistently observed in the skin aps of the control group, while antiVLA-4 reduced these parameters to a level similar to the sham group. These results indicate that anti-VLA-4 mAb may be used as an anti-in ammation agent, however the underlying mechanism still remains to be elucidated.

Monoclonal Antibody to Very Late Antigen-4 (VLA-4) Protects Skin Flaps against Ischemia-Reperfusion Injury: An Experimental Study in Rats