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Microglia are the major immune cells in the central nervous system and playa key role in brain injury pathology. However, the role of activated microgliaafter subacute cerebral ischemia (SCI) remains unknown. To address this issue,we established a permanent middle cerebral artery occlusion (pMCAO) rat modeland treated pMCAO rats with N-(6-oxo-5,6-dihydro-phenanthridin-2-yl)-N,N-dimethylacetamide(PJ34) (an inhibitor of microglial activation), or with vehicle alone. Finally,we determined the differences between the PJ34-and vehicle-treated rats with respectto neurological deficits, infarct volume, neuronal loss and the expression ofCD11b (a marker of microglial activation), glial cell line-derived neurotrophicfactor (GDNF) and tumor necrosis factor-α (TNF-α) at 1, 3 and 7 days after treatment.We found that the PJ34-treated rats had more severe neurological deficits anda larger infarct volume and exhibited a decreased CD11b expression, more neuronalloss, decreased expression of GDNF mRNA and protein but increased expression ofTNF-α mRNA and protein compared with the vehicle-treated rats at 3 and 7 daysafter treatment. These results indicate that activated microglia provide a neuroprotectiverole through balancing GDNF and TNF-α expression following SCI.

international journal of molecular medicine

Activated microglia provide a neuroprotective role by balancing glial cell-line derived neurotrophic factor and tumor necrosis factor-α secretion after subacute cerebral ischemia