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Luteolin Reduced the Traumatic Brain Injury-Induced Memory Impairments in Rats: Attenuating Oxidative Stress and Dark Neurons of Hippocampus



Ashaari Z1 ; Hassanzadeh G2, 3 ; Mokhtari T4, 5 ; Hosseini M1 ; Keshavarzi Z6 ; Amini M2 ; Bavarsad K1 ; Ijaz S2 ; Hadjzadeh MAR1, 7, 8
Authors
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Authors Affiliations
  1. 1. Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
  2. 2. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Nervous System Stem Cells Research Center, Semnan University of Medical Sciences, Semnan, Iran
  5. 5. Department of Anatomy, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran
  6. 6. Natural Products and Medicinal Plants Research Center, North Khorasan University of Medical Sciences, Bojnurd, Iran
  7. 7. Department of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
  8. 8. Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

Source: Acta Medica Iranica Published:2018

Abstract

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. © 2018 Tehran University of Medical Sciences. All rights reserved.