Evaluation of neuroprotective effects of Canna indica L against aluminium chloride induced memory impairment in rats

Background: Chronic stress elevates the cortisol beyond normal levels, which affects cognition including learning & memory. This injurious effect is primarily mediated via over excitation of metabotropic glucocorticoid receptors (mGR). Methods: The present study was aimed appraise the neuroprotective effects of naturally occurring molecule β-1,3-glucan by interfering with stress-cortisol-mGR axis. Our data of virtual screening (in silico) exhibited the promising interactions of βglucan with the mGR. Therefore, the study was extended to evaluate its efficacy (2.5, 5 and 10 mg/kg/ i.p) in an animal model of chronic unpredictable mild stress (CUMS, 28 days) induced memory impairment. Results: Results of the current study revealed the β-glucan provided dose dependent protection against deleterious effects of stress on learning and memory associated parameters observed in Morris water maze (MWM) task. At higher tested doses, it has also significantly antagonized the stress induced weight loss and corticosterone elevation. Conclusion: From these findings, it can be deduced that the β-glucan possesses therapeutic potential against stress induced memory impairment, and this effect can be attributed to its normalizing effect on corticosterone levels.

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Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain

Archives of Industrial Hygiene and Toxicology ◽

10.1515/aiht-2017-68-2878 ◽

2017 ◽

Vol 68 (1) ◽

pp. 27-37 ◽

Cited By ~ 20

Author(s):

Mahmoud M. Said ◽

Marwa M. Abd Rabo

Keyword(s):

Total Antioxidant Status ◽

Basal Diet ◽

Acetylcholinesterase Activity ◽

Aluminium Chloride ◽

Neuroprotective Effects ◽

Necrosis Factor Alpha ◽

Protein Levels ◽

Tnf Α ◽

Total Antioxidant ◽

Male Wistar Rats

AbstractAluminium (Al) is a neurotoxic metal that contributes to the progression of several neurodegenerative diseases. The aim of the present study was to evaluate the protective effect of dietary eugenol supplementation against aluminium (Al)- induced cerebral damage in rats. Male Wistar rats were divided into four groups: normal controls, rats fed a diet containing 6,000 μg g-1eugenol, rats intoxicated daily with aluminium chloride (84 mg kg-1body weight) p. o. and fed either a basal diet or a eugenol-containing diet. Daily oral administration of Al for four consecutive weeks to rats significantly reduced brain total antioxidant status (TAS) (11.42±0.31 μmol g-1tissue, p<0.001) with a subsequent significant enhancement of lipid peroxidation (MDA) (32.55±1.68 nmol g-1tissue, p<0.002). In addition, Al enhanced brain acetylcholinesterase activity (AChE) (46.22±4.90 U mg-1protein, p<0.001), tumour necrosis factor alpha (TNF-α) (118.72±11.32 pg mg-1protein, p<0.001), and caspase 3 (Casp-3) (8.77±1.26 ng mg-1protein, p<0.001) levels, and in contrast significantly suppressed brain-derived neurotrophic factor (BDNF) (82.74±14.53 pg mg-1protein, p<0.002) and serotonin (5-HT) (1.54±0.12 ng mg-1tissue, p<0.01) levels. Furthermore, decreased glial fibrillary acidic protein (GFAP) immunostaining was noticed in the striatum of Al-intoxicated rats, compared with untreated controls. On the other hand, co-administration of dietary eugenol with Al intoxication restored brain BDNF (108.76±2.64 pg mg-1protein) and 5-HT (2.13±0.27 ng mg-1tissue) to normal levels, enhanced brain TAS (13.43±0.24 μmol g-1tissue, p<0.05), with a concomitant significant reduction in TNF-α (69.98±4.74 pg mg-1protein) and Casp-3 (3.80±0.37 ng mg-1protein) levels (p<0.001), as well as AChE activity (24.50±3.25 U mg-1protein, p<0.001), and increased striatal GFAP immunoreactivity, compared with Al-treated rats. Histological findings of brain tissues verified biochemical data. In conclusion, eugenol holds potential as a neuroprotective agent through its hydrophobic, antioxidant, and anti-apoptotic properties, as well as its neurotrophic ability against Al-induced brain toxicity in rats.

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Neuroprotective Effects of Kangen-karyu on Spatial Memory Impairment in an 8-Arm Radial Maze and Neuronal Death in the Hippocampal CA1 Region Induced by Repeated Cerebral Ischemia in Rats

Journal of Pharmacological Sciences ◽

10.1254/jphs.08245fp ◽

2009 ◽

Vol 109 (3) ◽

pp. 424-430 ◽

Cited By ~ 15

Author(s):

Fengling Pu ◽

Kyoko Motohashi ◽

Tomohiro Kaneko ◽

Yurika Tanaka ◽

Naomi Manome ◽

...

Keyword(s):

Cerebral Ischemia ◽

Spatial Memory ◽

Neuronal Death ◽

Memory Impairment ◽

Radial Maze ◽

Neuroprotective Effects ◽

Ca1 Region ◽

Hippocampal Ca1 Region ◽

Hippocampal Ca1

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Neuroprotective effects of thymoquinone against MDMA-induced neurotoxicity

Research Journal of Pharmacy and Technology ◽

10.52711/0974-360x.2021.01033 ◽

2021 ◽

pp. 5945-5952

Author(s):

Mustafa NS. ◽

Mohamad N. ◽

Abu Bakar NH. ◽

Mohd Adnan LH. ◽

Jeharsae R. ◽

...

Keyword(s):

Memory Impairment ◽

Natural Compound ◽

Neuronal Damage ◽

Memory Performance ◽

Novel Object Recognition ◽

Psychoactive Substance ◽

Sprague Dawley ◽

Hippocampal Dentate Gyrus ◽

Object Recognition Test ◽

Neuroprotective Effects

MDMA (3, 4-methylenedioxymethamphetamine) is a psychoactive substance that is associated with neurotoxicity. MDMA exposure to human results in the degeneration of neuronal cells in the hippocampus. Hence, the purpose of this study was to examine the potential of a natural compound known as thymoquinone (TQ) to protect against neuronal damage and memory impairment in rats stimulated by MDMA. The administration of TQ into MDMA-induced neuronal damage rats was carried out in male Sprague Dawley via a 1-week treatment dividing into four groups (n=36, 7-9 per group). The studied groups involved with the treatments comprise i) Control (1 mL/kg saline), ii) MDMA (10 mg/kg MDMA), iii) MDMA+TQ (10 mg/kg MDMA + 40 mg/kg TQ) and iv) TQ control (40 mg/kg TQ). A novel object recognition test (NORT) was carried out to evaluate the memory performance of the rats, followed by a histopathological assessment of the hippocampal dentate gyrus. The histopathology analysis revealed a significant increase in numbers of positive cells by Fluoro-Jade C following the effect of MDMA on neuronal damage (MDMA induced group) compared to control (P<0.05). Next, the TQ treatments observed in MDMA+TQ exhibited a decline in positive cells from Fluoro-Jade C. The index of recognition memory was found to be increased in MDMA+TQ compared to the MDMA alone (P<0.05). This study suggests that the neuronal damage inflicted by MDMA in a rat model has the potential to be treated by TQ.

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