Lipocalin-2 in Stroke
Stroke is a sudden loss of neurological function due to ischemia or hemorrhage in the brain.
It is the fifth leading cause of death and a major cause of long-term disability in the United States.
There are two main types of stroke: ischemic and hemorrhagic strokes.
Ischemic stroke accounts for approximately 87% of all strokes and results from blockage of blood
flow into the brain by thrombus or embolus.
Hemorrhagic stroke, caused by rupture of cerebral blood vessels, is less common
than ischemic stroke but accounts for 50% of stroke death.
Currently, there is no proven medical or surgical treatment for hemorrhagic stroke.
Thrombolysis with fibrinolytic agents such as tissue Plasminogen Activator is
the only FDA approved therapy to reverse ischemic stroke.
However, only 5% of patients receive the treatment because tPA must be given within 3 to 4.5 hours after the occurrence of stroke. Delayed treatment may increase the risk of serious side effects such as hemorrhagic
transformation and reperfusion injury.
Ischemia initiates cerebral infarction during ischemic stroke, but reperfusion after
recanalization may promote secondary injury and worsen neurological outcomes.
Reperfusion injury includes a series of inflammatory events with activation and infiltration of circulating neutrophils, macrophages, and T-cells into infarcted brain tissue.
Post-stroke inflammation has detrimental effects, but may be needed for repairing
processes. In order to reduce stroke-reperfusion injury and develop effective and balanced
therapeutic methods, it is important to identify neurotoxic and neuroprotective molecules of
post-stroke inflammation.
In the acute stage of stroke, infiltrating immune cells release proinflammatory cytokines, chemokines,
reactive oxygen species, and matrix metalloproteinase, which amplify neuroinflammatory responses and lead to brain edema, neuronal death, and disruption of blood-brain barrier.
Neuro Open J. 2015; 2(1): 38-41. doi: 10.17140/NOJ-2-109
