Melatonin-induced neuroprotection after closed head injury is associated with increased brain antioxidants and attenuated late-phase activation of NF-κB and AP-1 1 SARA M. BENI, RON KOHEN * , RUSSEL J. REITER † , DUN-XIAN TAN † and ESTHER SHOHAMI 2 Departments of Pharmacology and * Pharmaceutics School of Pharmacy, The Hebrew University of Jerusalem, Jerusalem, Israel; and † Department of Cellular and Structural Biology, The University of Texas, San Antonio, Texas, USA 2 Correspondence: Department of Pharmacology, School of Pharmacy, The Hebrew University of Jerusalem, Jerusalem 91120, Israel. E-mail: esty@cc.huji.ac.il <h3>SPECIFIC AIMS</h3> Traumatic brain injury (TBI) leads to massive production of reactive oxygen species (ROS), which in turn mediates further secondary cellular damage. Our aim was to assess whether the neuroprotective effect of melatonin, a main pineal product with controversial antioxidant properties, involves redox-dependent mechanisms. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Effect of melatonin on clinical outcome and lesion size after CHI</h3> Mice were subjected to closed head injury (CHI) and 1 h later the initial Neurological Severity Score (NSS), composed of 10 behavioral and motor tests, was assessed. Immediately thereafter, vehicle or melatonin (1, 5, or 10 mg/kg) were administered intraperitoneally and NSS was reevaluated 24 h later. The dose
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Melatonin-induced neuroprotection after closed head injury is associated with increased brain antioxidants and attenuated late-phase activation of NF-κB and AP-1
BENI, SARA M.; KOHEN, RON; REITER, RUSSEL J.; TAN, DUN-XIAN; SHOHAMI, ESTHER
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, Volume 18 (1): 149
Fed of American Socs for Experimental Biology – Jan 1, 2004
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