Tehran University of Medical Sciences Acta Medica Iranica 0044-6025 56 9 2018 12 25 563 570 EN Zeinab Ashaari Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Gholamreza Hassanzadeh Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. AND Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran. Tahmineh Mokhtari Nervous System Stem Cells Research Center, Semnan University of Medical Sciences, Semnan, Iran. AND Department of Anatomy, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. Mahmoud Hosseini Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Zakieh Keshavarzi Natural Products and Medicinal Plants Research Center, North Khorasan University of Medical Sciences, Bojnurd, Iran. Mohsen Amini Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Kowsar Bavarsad Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Sahar Ijaz Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Mousa-Al-Reza Hadjzadeh Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. AND Department of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. AND Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. 2018 08 15 2018 09 11 Traumatic Brain Injury (TBI) is generally recognized as a major risk factor for memory impairments and Alzheimer’s disease (AD). In this experimental study, our aim was to investigate the ameliorating effects of luteolin (LUT) on the memory impairments, oxidative stress, and histopathological changes induced by TBI in rats. The adult male Wistar rats were randomly divided into six groups including: Control (Co), sham, TBI, TBI+LUT (10 mg/kg), TBI +LUT (25 mg/kg), TBI +LUT (50 mg/kg). To evaluate the protective effects of LUT on the memory of the rats, passive avoidance test using shuttle box was performed. Finally, the animals were anesthetized, and the brain tissues were removed and analyzed for oxidative stress parameters. Using histological methods, dark neuron production was also evaluated. There was a significant decrease in the latency time to enter the dark compartment in passive avoidance test in TBI animals. This latency time was significantly increased in TBI+LUT (25 mg/kg) and TBI+LUT (50 mg/kg) groups along with significant increases in superoxide dismutase and catalase activity in the hippocampal zone and a decrease in malondialdehyde (MDA). The number of dark neurons in the hippocampus decreased with all three doses of LUT. In the present study, LUT showed neuroprotective effects, improvement in learning and reduction in memory impairment induced by TBI in rats. Protection against oxidative stress might be a possible mechanism behind these effects. Further works are necessary to work out if LUT is potentially a suitable therapeutic candidate for neural disorders. https://acta.tums.ac.ir/index.php/acta/article/view/7437 https://acta.tums.ac.ir/index.php/acta/article/download/7437/5154