TABLE 2.

Expression of LCN2 in the plasma and brain of stroke patients and stroke-induced animal models.

Type of stroke	Model	LCN2 level	Function/Clinical correlation
Ischemic stroke	tMCAO	↑	LCN2 cause brain injury
			LCN2 released by injured neurons as a help me distress signal that activates microglia and astrocytes into potentially pro-recovery phenotypes.
			LCN2 deficiency attenuates neuroinflammation and brain injury
			LCN2 mainly comes from astrocytes and induce proinflammatory cytokines expression under hypoxic conditions
			LCN2 is an infection-related biomarker to predict clinical outcome in ischemic stroke
	pMCAO	↑	LCN2 null mice did not show any protection
	OGD	↑	LCN2 induce astrocytes activation and polarization
	Carotid artery injury	↑	LCN2 interacts with MMP9 may modulate MMP9 proteolytic activity in the vascular repair process
Hemorrhagic stroke	ICH	↑	LCN2 cause brain injury and up-regulation of ferritin
			LCN2 enhance PRDX2 induced brain injury
			Increased LCN2 may relate to clear iron after ICH
			Thrombin induce the expression of LCN2 through PAR-1 and cause brain injury
	IVH	↑	LCN2 promote M1 polarization in LPS induced brain injury
			LCN2 induce high portality and more ventricular dilation
	SAH	↑	LCN2 induce whiter matter injury after SAH
			LCN2 deletion attenuates MRI and pathological changes in whiter matter after SAH
			LCN2 increases early after SAH and is associated with neuroinflammation and unfavorable outcome
		NA	LCN2 deficiency decreased the number of cerebral thromboembolism

tMCAO, transient middle cerebral artery occlusion; pMCAO, permanent middle cerebral artery occlusion; OGD, oxygen-glucose deprivation; ICH, intracerebral hemorrhage; IVH, intraventricular hemorrhage; SAH, subarachnoid hemorrhage; MMP9, matrix metallopeptidase 9; PRDX2, peroxiredoxin 2; PAR-1, protease activated receptor 1; LPS, lipopolysaccharide; NA, not applicable.