Naringenin ameliorates learning and memory impairment following systemic lipopolysaccharide challenge in the rat

Khajevand-Khazaei, M.-R. and Ziaee, P. and Motevalizadeh, S.-A. and Rohani, M. and Afshin-Majd, S. and Baluchnejadmojarad, T. and Roghani, M. (2018) Naringenin ameliorates learning and memory impairment following systemic lipopolysaccharide challenge in the rat. European Journal of Pharmacology, 826. pp. 114-122.

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Systemic inflammation following infection is usually associated with long-term complications including cognitive deficit and dementia. Neuroinflammation and cognitive decline are also main hallmarks of several neurological conditions. Naringenin is a citrus flavanone with anti-inflammatory, neuroprotective, and antioxidant potential. In this study, the protective effect of naringenin against lipopolysaccharide (LPS)-induced cognitive decline was evaluated in the rat. LPS was daily injected at a dose of 167 μg/kg for 1 week and naringenin was administered p.o. at doses of 25, 50, or 100 mg/kg/day. Treatment of LPS-injected rats with naringenin dose-dependently improved spatial recognition memory in Y maze, discrimination ratio in novel object discrimination task, and retention and recall capability in passive avoidance test. Furthermore, naringenin lowered hippocampal malondialdehyde (MDA) as an index of lipid peroxidation and improved antioxidant defensive system comprising superoxide dismutase (SOD), catalase, and glutathione (GSH) in addition to decreasing acetylcholinesterase (AChE) activity. Additionally, naringenin was able to lower hippocampal nuclear factor-kappaB (NF-κB), toll-like receptor 4 (TLR4), tumor necrosis factor α (TNFα), cyclooxygenase-2 (COX2), inducible nitric oxide synthase (iNOS), glial fibrillary acidic protein (GFAP) level and its immunoreactivity, and to elevate nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Taken together, naringenin could alleviate LPS-induced cognitive deficits and neuroinflammation, as was evident from attenuation of oxidative stress and AChE and modulation of Nrf2/NF-κB/TNFα/COX2/iNOS/TLR4/GFAP. © 2018 Elsevier B.V.

Item Type: Article
Additional Information: cited By 3
Uncontrolled Keywords: acetylcholinesterase; catalase; cyclooxygenase 2; dexamethasone; glial fibrillary acidic protein; glutathione; immunoglobulin enhancer binding protein; inducible nitric oxide synthase; lipopolysaccharide; malonaldehyde; naringenin; superoxide dismutase; toll like receptor 4; transcription factor Nrf2; tumor necrosis factor; flavanone derivative; naringenin; neuroprotective agent, animal cell; animal experiment; animal model; animal tissue; Article; attenuation; brain level; cognitive defect; controlled study; dose response; drug activity; drug dose comparison; drug effect; enzyme activity; hippocampus; immunoreactivity; learning disorder; lipid peroxidation; male; maze test; memory disorder; nervous system inflammation; neuromodulation; nonhuman; oxidative stress; passive avoidance test; priority journal; protein expression level; rat; recall; Wistar rat; animal; cognitive defect; disease model; human; immunology; inflammation; metabolism; short term memory; spatial memory, Acetylcholinesterase; Animals; Cognition Disorders; Disease Models, Animal; Dose-Response Relationship, Drug; Flavanones; Hippocampus; Humans; Inflammation; Lipopolysaccharides; Male; Maze Learning; Memory, Short-Term; Neuroprotective Agents; Oxidative Stress; Rats; Rats, Wistar; Spatial Memory
Subjects: WM Psychiatry
Depositing User: eprints admin
Date Deposited: 30 Dec 2018 07:06
Last Modified: 21 Aug 2019 09:35

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