Neuroprotection induced by N-acetylcysteine and selenium against traumatic brain injury-induced apoptosis and calcium entry in hippocampus of rat.
RatTBIUnspecifiedSprague-Dawleymalen = 32 rats divided into four groupsIntraperitonealFirst dose 1 h after injury
Model: Traumatic brain injury model with hippocampal neuron isolation at 3 days
Both agents lowered hippocampal calcium entry, reactive oxygen species, apoptosis and caspase activity after injury, with N-acetylcysteine appearing more effective than selenium.
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