The protective effect of a L-type calcium channel blocker, nimodipine, on cell injury induced by oxygen-glucose deprivation (OGD) in PC12 cells was investigated. PC12 cells were exposed to in-vitro oxygen-glucose deprivation (30 minutes and 60 minutes respectively) in the presence or absence of nimodipine (10mM/L) in three different time schedules (pre-24h, pre-3h and concurrently). Cellular vi...

In vitro ischemia models have utilized oxygen, or oxygen and glucose deprivation to simulate ischemic neuronal injury. Combined oxygen and glucose deprivation can induce neuronal damage which is in part mediated through NMDA receptors. Severe oxygen deprivation alone however can cause neuronal injury which is not NMDA mediated. We tested the hypothesis that NMDA, or non-NMDA receptor mediated m...

To determine the role of calcium homeostasis in ischemic neuronal death, the authors used an in vitro model of oxygen-glucose deprivation in neuronal cell lines. Exposure of human neuroblastoma SH-SY5Y cells to 10-to 16-hour oxygen-glucose deprivation decreased viability to 50% or less, and longer exposure times killed almost all cells. The death following 10-to 16-hour oxygen-glucose deprivati...

We investigated the effects of 25Mg-Porphyrin-Fullerene nanoparticles, (25MgPMC16) smart ferroporphyrin nanoparticles, on PC12 cells exposed to oxygen-glucose deprivation/reperfusion. In order to explore its effect on cells under oxygen-glucose deprivation conditions, the cultures were pretreated with 25MgPMC16 24 hours prior to oxygen-glucose deprivation/reperfusion. To initiate the oxygen-glu...

We examined the effects of secobarbital and other sedative-hypnotic barbiturates on the neuronal death induced by exposure to excitatory amino acids or deprivation of oxygen or glucose in mouse cortical cell cultures. N-Methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4- isoxazolepropionate, and kainate toxicities were attenuated in a concentration-dependent fashion by high concentrati...