Ischemic and hemorrhagic strokes have different etiologies, but share some pathogenic mechanisms, including a pro-neurotoxic effect of endogenous tissue plasminogen activator (tPA) via N-methyl-d-Aspartate (NMDA) receptors. Thus, in a model of intracerebral hemorrhage in rats, we investigated the therapeutic value of a strategy of immunotherapy (αATD-GluN1 antibody) preventing the interaction of tPA with NMDA receptors. We found that a single intravenous injection of αATD-GluN1 reduced brain edema, neuronal death, microglial activation and functional deficits following intracerebral hemorrhage, without affecting the hematoma volume.
- Antibodies, Monoclonal, Murine-Derived/administration & dosage
- Intracranial Hemorrhages/immunology
- Random Allocation
- Rats, Sprague-Dawley
- Receptors, N-Methyl-D-Aspartate/metabolism
- Tissue Plasminogen Activator/antagonists & inhibitors
- Treatment Outcome