Influence of Inflammation on Poststroke Plasticity

Table 1

Examples of anti-inflammatory strategies effective in experimental stroke.

Target mediator in inflammatory cascade	Therapeutic intervention	Outcome	Literature examples
General inflammation	Minocycline	Attenuation of ischemic deficits are inhibition of apoptotic neuronal cell death after MCAO. Better outcome from stroke in patients	[54–56, 78]
	Intravenous immunoglobulin therapy	Elimination of mortality and reduction of brain damage after MCAO in mice	[58, 59]
Complement inhibition	Cobra venom factor (CVF)	Reduced infarct and atrophy are improved clinical outcome	[79, 80]
	C1 inhibition: C1-INH	Neuroprotection	[81]
	C3 inhibition: sCR1, C3 KO	Reduced infarct volume and neurological deficit score	[82, 83]
	C5 inhibition: C5 KO	Improvement of functional outcome, reduced brain damage	[58]
Leukocytes	Neutrophil inhibitory factor	Neuroprotection after focal ischemia in rats and reduction of the number of infiltrated neutrophils and infarct volume	[84, 85]
Lymphocytes T	Sphingosine 1-phosphate receptor agonist FTY720 (Fingolimod)	Reduction of infarct volume and cell death and improvement of neurological score after MCAO in rats	[57, 86, 87]
Prostaglandins	Cyclooxygenase pathway: Ibuprofen	Restoration of plasticity in visual and somatosensory cortex after photothrombotic stroke in mice without the neuroprotective effect	[35, 36]
	COX-2 KO	Reduction in the brain injury after MCAO in mice	[88]
Cytokines	IL-1:
	IL-1 receptor antagonist	Administration of human interleukin-1 receptor antagonist reduced damage caused by MCAO in rats	[64, 66]
	IL-1 KO	70% reduction of infarct volume after MCAO	[65, 89, 90]
	IL-1R1 null mice	reduced brain damage and increased neuronal survival after ligation of right common carotid artery in mice	[91]
	TNFα:
	Anti-TNF antibodies	Blocking endogenous TNF-alpha reduced focal ischemic brain injury in mice and rats after MCAO	[62, 92]
	TNF decoy receptor	Reduction of stroke volume, neural deficits, extent of microglial cell activation, and apoptotic cell death after MCAO in mice	[93, 94]
	Soluble TNFα receptor (TNFbp)	Reduction of infarct size after MCAO in mice	[75]