Abstract
Oxidative stress and inflammation can be involved in cognitive dysfunction associated with neurodegenerative disorders. Diazepam (DZP) administration has been chosen to simulate the memory impairment. The aim of this study was to evaluate the effects of curcumin (CUR) on spatial cognition, ambulatory activity, and blood and brain oxidative stress levels. The ERK/NF-κB signaling pathway and the histopathological changes in the hippocampus and frontal lobe, in diazepam-treated rats, were also analyzed. The animals were divided into 4 groups: control, carboxymethylcellulose (CMC) + CUR, CMC + DZP, and CUR + CMC + DZP. CUR (150 mg/kg b.w.) was orally administered for 28 days. DZP (2 mg/kg b.w.) was intraperitoneally administered 20 minutes before the behavioral tests (open field test, Y-maze, and elevated plus maze). CUR improved the spontaneous alternation behavior, decreased the oxidative stress levels, both in the blood and in the hippocampus, and downregulated the extracellular signal-regulated kinase (ERK 1/2)/nuclear transcription factor- (NF-) κB/pNF-κB pathway in the hippocampus and the iNOS expression in the hippocampus and frontal lobe of the DZP-treated rats. Histopathologically, no microscopic changes were found. The immunohistochemical signal of iNOS decreased in the DZP and CUR-treated group. Thus, our findings suggest that curcumin administration may improve the cognitive performance and may also have an antioxidant effect.
Highlights
Memory, one of the most complex brain functions, involving multiple neuronal pathways and neurotransmitters, is considered the ability of an individual to record, retain, and recall the information when needed [1, 2].Aging, stressful conditions, reduced brain metabolism, high oxidative stress levels, inflammation, or reduced plasticity has been hypothesized to be involved in cognitive dysfunction associated with neurodegenerative disorders, such as Alzheimer’s (AD) or Parkinson’s disease (PD) [3,4,5]
Curcumin (CUR), Bradford reagent, trichloroacetic acid, and o-phthalaldehyde were obtained from Sigma-Aldrich Chemicals GmbH (Germany), and diazepam (DZP) (10 mg/2 mL) was purchased from Terapia Ranbaxy, Cluj-Napoca. 2-Thiobarbituric acid and EDTA-Na2 were obtained from Merck KGaA (Darmstadt, Germany) while absolute ethanol and n-butanol were from Chimopar (Bucharest, Romania)
Our results showed that total travelled distance and travelled distance in the periphery were significantly increased in the diazepam and curcumin group as compared to those of the control group (p < 0 05)
Summary
One of the most complex brain functions, involving multiple neuronal pathways and neurotransmitters, is considered the ability of an individual to record, retain, and recall the information when needed [1, 2]. Curcumin downregulates various proinflammatory intracellular systems such as NF-κB, inducible nitric oxide synthase (iNOS), hypoxia-inducible factor-1, and proinflammatory cytokine such as: interleukin- (IL-) 6, IL-1β, and tumor necrosis factor- (TNF-) α It exerts antiapoptotic function by overexpression of Bcl-2 and decrease of the bax/Bcl-2 ratio. Side effects of the BZDs, such as sedation and anterograde amnesia, are α1 mediated [22, 24] Based on these data, our study intended to evaluate the effect of a high dose of DZP on spatial cognition in conjunction with oxidative stress, ERK 1/2/NF-κB signaling pathway, and histopathological changes in the hippocampus, frontal lobe, and whole brain and the impact of curcumin pretreatment on these parameters in rats
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