scholarly journals Neuroprotective Effects ofCentella asiaticaagainst Intracerebroventricular Colchicine-Induced Cognitive Impairment and Oxidative Stress

2009 ◽  
Vol 2009 ◽  
pp. 1-8 ◽  
Author(s):  
Anil Kumar ◽  
Samrita Dogra ◽  
Atish Prakash
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Oxidative Damage ◽  
Memory Impairment ◽  
Memory Performance ◽  
Centella Asiatica ◽  
Acetylcholinesterase Activity ◽  
Early Event ◽  
Neuroprotective Effects ◽  
Male Wistar Rats

Oxidative stress appears to be an early event involved in the pathogenesis of Alzheimer's disease. The present study was designed to investigate the neuroprotective effects ofCentella asiaticaagainst colchicine-induced memory impairment and oxidative damage in rats. Colchicine (15 μg/5 μL) was administered intracerebroventricularly in the lateral ventricle of male wistar rats. Morris water maze and plus-maze performance tests were used to assess memory performance tasks. Various biochemical parameters such as lipid peroxidation, nitrite, reduced glutathione, glutathione-S-transferase, superoxide dismutase, acetylcholinesterase were also assessed. ICV colchicine resulted marked memory impairment and oxidative damage. Chronic treatment withCentella asiaticaextract (150 and 300 mg/kg, p.o.) for a period of 25 days, beginning 4 days prior to colchicine administration, significantly attenuated colchicine-induced memory impairment and oxidative damage. Besides,Centella asiaticasignificantly reversed colchicines administered increase in acetylcholinesterase activity. Thus, present study indicates protective effect ofCentella asiaticaagainst colchicine-induced cognitive impairment and associated oxidative damage.

scholarly journals NEUROPROTECTIVE EFFECT OF CITRULLUS LANATUS SEED EXTRACTS ON CEREBRAL ISCHEMIC REPERFUSION INJURY INDUCED COGNITIVE IMPAIRMENT AND OXIDATIVE STRESS

2019 ◽  
pp. 38-44
Author(s):  
Girija Pashikanti ◽  
MAKULA AJITHA ◽  
GOVERDHAN PUCHCHAKAYALA
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Citrullus Lanatus ◽  
Neuroprotective Effect ◽  
Memory Performance ◽  
Albino Rats ◽  
Early Event ◽  
Neuroprotective Effects ◽  
Aqueous Fraction ◽  
And Oxidative Stress

Objective: Oxidative stress appears to be an early event involved in the pathogenesis of Alzheimer's disease (AD). The present study was designed to investigate the neuroprotective effects of citrullus lanatus on bilateral common carotid artery occlusion (BCCAO) induced cognitive impairment and oxidative stress in Wistar albino rats. Methods: Cognitive impairment and oxidative stress were induced by BCCAO for 30 min, followed by 7 d reperfusion of male wistar rats. Morris water maze and rectangular maze performance tests and locomotor activity were used to assess memory performance tasks. To study the activity, rats weighing 250-300g were pre-treated with successive extracts of n-hexane fraction (HF), ethyl acetate fraction (EAF), ethanol fraction (EF) and aqueous fraction (AF) of 400 mg/kg, 200 mg/kg, p. o of each for 10 d and the treatment was continued for another 7 d after cerebral ischemia. Various biochemical parameters like lipid peroxidation, Catalase, DPPH and AchE were also estimated in the brain after the treatment. Results: There was significantly increased oxidative stress and cholinesterase activity with cognitive decline in the hippocampus in rats of BCCAO group as compared to sham-operated (p<0.05). The animals treated with Donepezil, HF and EF prevented the biochemical changes significantly (p<0.001) and there was significant (p<0.001) improvement in cognitive parameters compared to BCCAO treated rats. Conclusion: Thus present study indicates the neuroprotective effect of citrulus lanatus seed extract (HF and EF) against BCCAO induced cognitive impairment and associative oxidative damage.

scholarly journals Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain

2017 ◽  
Vol 68 (1) ◽  
pp. 27-37 ◽  
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.

scholarly journals Ethanol Extract of Maclura tricuspidata Fruit Protects SH-SY5Y Neuroblastoma Cells against H2O2-Induced Oxidative Damage via Inhibiting MAPK and NF-κB Signaling

2021 ◽  
Vol 22 (13) ◽  
pp. 6946
Author(s):  
Weishun Tian ◽  
Suyoung Heo ◽  
Dae-Woon Kim ◽  
In-Shik Kim ◽  
Dongchoon Ahn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Oxidative Damage ◽  
Cell Damage ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Biologically Active ◽  
Mitogen Activated Protein Kinase ◽  
Protective Effects ◽  
Neuroprotective Effects

Free radical generation and oxidative stress push forward an immense influence on the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Maclura tricuspidata fruit (MT) contains many biologically active substances, including compounds with antioxidant properties. The current study aimed to investigate the neuroprotective effects of MT fruit on hydrogen peroxide (H2O2)-induced neurotoxicity in SH-SY5Y cells. SH-SY5Y cells were pretreated with MT, and cell damage was induced by H2O2. First, the chemical composition and free radical scavenging properties of MT were analyzed. MT attenuated oxidative stress-induced damage in cells based on the assessment of cell viability. The H2O2-induced toxicity caused by ROS production and lactate dehydrogenase (LDH) release was ameliorated by MT pretreatment. MT also promoted an increase in the expression of genes encoding the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). MT pretreatment was associated with an increase in the expression of neuronal genes downregulated by H2O2. Mechanistically, MT dramatically suppressed H2O2-induced Bcl-2 downregulation, Bax upregulation, apoptotic factor caspase-3 activation, Mitogen-activated protein kinase (MAPK) (JNK, ERK, and p38), and Nuclear factor-κB (NF-κB) activation, thereby preventing H2O2-induced neurotoxicity. These results indicate that MT has protective effects against H2O2-induced oxidative damage in SH-SY5Y cells and can be used to prevent and protect against neurodegeneration.

scholarly journals Tualang Honey Attenuates Noise Stress-Induced Memory Deficits in Aged Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Khairunnuur Fairuz Azman ◽  
Rahimah Zakaria ◽  
Che Badariah Abdul Aziz ◽  
Zahiruddin Othman
Keyword(s):  
Oxidative Stress ◽  
Memory Performance ◽  
Acetylcholinesterase Activity ◽  
Protein Carbonyl ◽  
Protective Effects ◽  
Aged Rats ◽  
Stress Exposure ◽  
Object Recognition Test ◽  
Noise Stress ◽  
Tualang Honey

Ageing and stress exposure may lead to memory impairment while oxidative stress is thought to be one of the underlying mechanisms involved. This study aimed to investigate the potential protective effects of Tualang honey supplementation on memory performance in aged rats exposed to noise stress. Tualang honey supplementation was given orally, 200 mg/kg body weight for 28 days. Rats in the stress group were subjected to loud noise, 100 dB(A), 4 hours daily for 14 days. All rats were subjected to novel object recognition test for evaluation of memory performance. It was observed that the rats subjected to noise stress exhibited significantly lower memory performance and higher oxidative stress as evident by elevated malondialdehyde and protein carbonyl levels and reduction of antioxidant enzymes activities compared to the nonstressed rats. Tualang honey supplementation was able to improve memory performance, decrease oxidative stress levels, increase brain-derived neurotrophic factor (BDNF) concentration, decrease acetylcholinesterase activity, and enhance neuronal proliferation in the medial prefrontal cortex (mPFC) and hippocampus. In conclusion, Tualang honey protects against memory decline due to stress exposure and/or ageing via enhancement of mPFC and hippocampal morphology possibly secondary to reduction in brain oxidative stress and/or upregulation of BDNF concentration and cholinergic system.

Neuroprotective effects of thymoquinone against MDMA-induced neurotoxicity

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.

scholarly journals 17β-Estradiol Modulates SIRT1 and Halts Oxidative Stress-Mediated Cognitive Impairment in a Male Aging Mouse Model

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 928 ◽  
Author(s):  
Mehtab Khan ◽  
Rahat Ullah ◽  
Shafiq Ur Rehman ◽  
Shahid Ali Shah ◽  
Kamran Saeed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Mouse Model ◽  
Memory Impairment ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ros Generation ◽  
Dependent Manner ◽  
Molecular Docking Study ◽  
17Β Estradiol

Oxidative stress has been considered the main mediator in neurodegenerative disease and in normal aging processes. Several studies have reported that the accumulation of reactive oxygen species (ROS), elevated oxidative stress, and neuroinflammation result in cellular malfunction. These conditions lead to neuronal cell death in aging-related neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease. Chronic administration of d-galactose (d-gal) for a period of 10 weeks causes ROS generation and neuroinflammation, ultimately leading to cognitive impairment. In this study, we evaluated the estrogen receptor α (ERα)/silent mating type information regulation 2 homolog 1 (SIRT1)-dependent antioxidant efficacy of 17β-estradiol against d-gal-induced oxidative damage-mediated cognitive dysfunction in a male mouse model. The results indicate that 17β-estradiol, by stimulating ERα/SIRT1, halts d-gal-induced oxidative stress–mediated JNK/NF-ҡB overexpression, neuroinflammation and neuronal apoptosis. Moreover, 17β-estradiol ameliorated d-gal-induced AD-like pathophysiology, synaptic dysfunction and memory impairment in adult mouse brains. Interestingly, inhibition of SIRT1 with Ex527 (a potent and selective SIRT1 inhibitor) further enhanced d-gal-induced toxicity and abolished the beneficial effect of 17β-estradiol. Most importantly, for the first time, our molecular docking study reveals that 17β-estradiol allosterically increases the expression of SIRT1 and abolishes the inhibitory potential of d-ga. In summary, we can conclude that 17β-estradiol, in an ERα/SIRT1-dependent manner, abrogates d-gal-induced oxidative stress–mediated memory impairment, neuroinflammation, and neurodegeneration in adult mice.

Neuroprotective effects of dietary supplement Kang-fu-ling against high-power microwave through antioxidant action

2014 ◽  
Vol 5 (9) ◽  
pp. 2243-2251 ◽  
Author(s):  
Shaohua Hu ◽  
Ruiyun Peng ◽  
Changzhen Wang ◽  
Shuiming Wang ◽  
Yabing Gao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Protective Effect ◽  
Dietary Supplement ◽  
High Power ◽  
Antioxidant Action ◽  
Histopathological Changes ◽  
Neuroprotective Effects ◽  
High Power Microwave ◽  
Power Microwave

KFL displays a protective effect against HPM-induced cognitive impairment and histopathological changes by ameliorating oxidative stress via the Nrf2-ARE signaling pathway.

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