Abstract
Injury to the central nervous system initiates complex physiological, cellular and molecular processes that can result in neuronal cell death. Of interest to this review is the activation of the kinin family of neuropeptides, in particular bradykinin and substance P. These neuropeptides are known to have a potent pro-inflammatory role and can initiate neurogenic inflammation resulting in vasodilation, plasma extravasation and the subsequent development of edema. As inflammation and edema play an integral role in the progressive secondary injury that causes neurological deficits, this review critically examines kinin receptor antagonists as a potential neuroprotective intervention for acute brain injury, and more specifically, traumatic brain and spinal cord injury and stroke.
Highlights
Injuries to the central nervous system (CNS) initiate a complex cascade of secondary biochemical and molecular events that can exacerbate the initial primary injury and the resultant neurological deficits [1]
This study showed the ability of Anatibant® to cross the normal blood-brain barrier (BBB) and displace the B2 receptor radioligand from various regions including the forebrain, basal ganglia and hindbrain
A magnesium deficient diet in these animals is known to induce neurogenic inflammation with associated increases in substance P (SP) and proinflammatory cytokines [116]. These results suggest that administration of a NK1 antagonist during ischemic injury may provide a novel avenue for neuroprotection following ischemic stroke
Summary
Injuries to the central nervous system (CNS) initiate a complex cascade of secondary biochemical and molecular events that can exacerbate the initial primary injury and the resultant neurological deficits [1]. Many factors that contribute to the secondary phase of injury have been identified including blood-brain barrier (BBB) disruption, edema formation, release of neurotoxic excitatory amino acids, oxidative stress and apoptosis, amongst others. The ability of pharmacological agents to limit the biochemical neurotoxicity and secondary cell death has been well established in numerous animal models of traumatic brain injury (TBI), spinal cord injury (SCI) and stroke. If a target could be identified that has modulatory effects on multiple injury factors, this target could theoretically provide a multipotential therapeutic approach. One such target is the kinin family of neuropeptides that have been shown to be important modulators of acute CNS injury through multiple mechanisms
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