Bradykinin antagonist decreases early disruption of the blood–spinal cord barrier after spinal cord injury in mice

Abstract

Bradykinin is one of the key molecules involved in the disruption of the blood–brain barrier and blood–spinal cord barrier occurring after spinal cord injury (SCI). Previously we have shown a biphasic opening of the blood–spinal cord barrier as well as increased transport of tumor necrosis factor-α (TNFα) after SCI by compression of the lumbar spinal cord in mice. To evaluate the role of bradykinin in the two phases of blood–spinal cord barrier disruption, we pretreated mice with a potent bradykinin antagonist, the decapeptide B9430, before SCI. Our results show that B9430 decreased the general blood–spinal cord barrier disruption occurring immediately after SCI but failed to affect the delayed opening of the blood–spinal cord barrier observed 72 h after SCI. By contrast, the entry of TNFα after SCI was not affected by B9430 treatment. We conclude that bradykinin is involved in the early phase of blood–spinal cord barrier disruption, with B9430 non-selectively blocking this early disruption without affecting the selective transport system for TNFα. This indicates the therapeutic potential of bradykinin antagonists in ameliorating tissue damage induced by SCI.