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      Immediate and delayed treatments with curcumin prevents forebrain ischemia-induced neuronal damage and oxidative insult in the rat hippocampus.

      Neurochemical Research

      Animals, Antioxidants, metabolism, Apoptosis, Brain Ischemia, pathology, Catalase, Curcumin, therapeutic use, Enzyme Inhibitors, Glutathione, Hippocampus, cytology, Humans, Iron, Lipid Peroxidation, Male, Malondialdehyde, Neurons, Neuroprotective Agents, Oxidative Stress, Prosencephalon, Rats, Rats, Wistar, Superoxide Dismutase

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          Oxidative stress is believed to contribute to neurodegeneration following ischemic injury. The present study was undertaken to evaluate the possible antioxidant neuroprotective effect of curcumin (Cur) on neuronal death of hippocampal CA1 neurons following transient forebrain ischemia in rat. Treatment of Cur (200 mg/kg/day, i.p.) at three different times (immediately, 3 h and 24 h after ischemia) significantly (P<0.01) reduced neuronal damage 7 days after ischemia. Also, treatment of ischemic rats with Cur decreased the elevated levels of MDA and increased GSH contents, catalase and SOD activities to normal levels. In the in vitro, Cur was as potent as antioxidant (IC(50) = 1 microM) as butylated hydroxytoluene. The present study demonstrates that curcumin treatment attenuates forebrain ischemia-induced neuronal injury and oxidative stress in hippocampal tissue. Thus treatment with curcumin immediately or even delayed until 24 h may have the potential to be used as a protective agent in forebrain ischemic insult in human.

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