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

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 change...

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Bibliographic Details
Published inActa medica Iranica Vol. 56; no. 9; p. 563
Main Authors Ashaari, Zeinab, Hassanzadeh, Gholamreza, Mokhtari, Tahmineh, Hosseini, Mahmoud, Keshavarzi, Zakieh, Amini, Mohsen, Kowsar Bavarsad, Ijaz, Sahar, Mousa-Al-Reza, Hadjzadeh
Format Journal Article
LanguageEnglish
French
Published Tehran Tehran University of Medical Sciences 2018
Subjects
Animal cognition
Antioxidants
Behavioral sciences
Brain research
Drug dosages
Enzymes
Herbal medicine
Laboratory animals
Learning and memory
Luteolin
Medical research
Medicine
Memory
Neurons
Oxidative stress
Rat
Research centers
Studies
Traumatic brain injury
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Summary: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.
ISSN:0044-6025
1735-9694