Hypoxia/ischemia induces microglial activation and the release of pro-inflammatory cytokines and neurotoxic factors. (A-C) BV-2 cells were exposed to oxygen-glucose deprivation (OGD), and the mRNA levels of the pro-inflammatory cytokines (A)tumor necrosis factor (TNF)-α, (B) interleukin (IL)-1β and (C)inducible nitric oxide synthase (iNOS) were evaluated using real-time PCR at 3 hoursafter OGD treatment. (D-E) The release of(D) TNF-α (E) and IL-1β into the medium of BV-2 cells was measured by ELISA at 48 hours after OGD. (F) The release of NO into the medium of BV-2 cells was measured by the Griess assay. Results are presented as the mean ± SE from three independent experiments. (G) Brain homogenates were obtained from the hippocampus 3 daysafter transient global cerebral ischemia/reperfusion (I/R) injury. The supernatant concentrations of IL-1β and TNF-α were tested by ELISA. (H) Sections from rat brain taken 3 daysafter I/R injury were incubated with primary antibodies against CD11b and iNOS. Representative immunoreactivities in the hippocampal CA1 region are shown. Photomicrographs are shown at ×400 magnification. ‘Ctrl’ (control) represents the microglial cells that were not subjected to OGD treatment. *P < 0.05.