Table 1: Mediators of microglial activation after cerebral ischemia and intracerebral hemorrhage.

MediatorMeasurements usedResultsCitation

Ischemic stroke
Galectin 3Galectin 3−/− mice subjected to 60-minute MCAO followed by reperfusion for either 24 or 72 hoursGalectin 3 reduces cell death and infarct volume [23]
NotchPrimary cell cultures and in  vivo models of microglial activation (LPS) and MCAO in antisense Notch miceNotch leads to increased neuroinflammation[44]
SPARCFocal photothrombotic model of ischemic stroke in SPARC−/− miceSPARC−/− microglia have increased processes length and branching and increased microgliosis[45]
HMGB1shRNA and HMGB1 inhibitor used to knock down HMGB1 in ischemic stroke model and primary microglial culturesHMGB1 promotes neuroinflammation[4648]
CX3CL1Behavioral outcomes, edema, peripheral cell infiltration, cytokine production in CX3CR1 knockout mice in 30- and 60-minute MCAOCX3CL1-CX3CR1 signaling leads to worse functional outcome and higher neuroinflammation[4954]

Intracerebral hemorrhage
ThrombinThrombin injection in rats and in culture caused neuronal apoptosis and increased cytokine productionActivates microglia and promotes cytokine production[5560]
HemeBlood or hemin injectionActivates microglia and leads to neuroinflammation[6163]

SPARC: secreted protein acidic rich in cysteine; HMGB1: high mobility group box 1.