scholarly journals Analogous β-Carboline Alkaloids Harmaline and Harmine Ameliorate Scopolamine-Induced Cognition Dysfunction by Attenuating Acetylcholinesterase Activity, Oxidative Stress, and Inflammation in Mice

2018 ◽  
Vol 9 ◽  
Author(s):  
Shu-Ping Li ◽  
Yu-Wen Wang ◽  
Sheng-Lan Qi ◽  
Yun-Peng Zhang ◽  
Gang Deng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acetylcholinesterase Activity ◽  
Cognition Dysfunction

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.

scholarly journals Comparative study of oxidative stress parameters and acetylcholinesterase activity in the liver of Pelophylax esculentus complex frogs

2017 ◽  
Vol 24 (1) ◽  
pp. 51-58 ◽  
Author(s):  
Marko Prokić ◽  
Slavica Borković-Mitić ◽  
Imre Krizmanić ◽  
Jelena Gavrić ◽  
Svetlana Despotović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Comparative Study ◽  
Acetylcholinesterase Activity ◽  
Oxidative Stress Parameters ◽  
Pelophylax Esculentus ◽  
Stress Parameters

scholarly journals Astragalus Polysaccharide Suppresses 6-Hydroxydopamine-Induced Neurotoxicity in Caenorhabditis elegans

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Haifeng Li ◽  
Ruona Shi ◽  
Fei Ding ◽  
Hongyu Wang ◽  
Wenjing Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Protective Effect ◽  
Therapeutic Potential ◽  
Neuroprotective Effect ◽  
Acetylcholinesterase Activity ◽  
Apoptosis Pathway ◽  
Acidic Polysaccharide ◽  
C Elegans ◽  
6 Hydroxydopamine

Astragalus membranaceus is a medicinal plant traditionally used in China for a variety of conditions, including inflammatory and neural diseases. Astragalus polysaccharides are shown to reduce the adverse effect of levodopa which is used to treat Parkinson’s disease (PD). However, the neuroprotective effect of Astragalus polysaccharides per se in PD is lacking. Using Caenorhabditis elegans models, we investigated the protective effect of astragalan, an acidic polysaccharide isolated from A. membranaceus, against the neurotoxicity of 6-hydroxydopamine (6-OHDA), a neurotoxin that can induce parkinsonism. We show that 6-OHDA is able to degenerate dopaminergic neurons and lead to the deficiency of food-sensing behavior and a shorter lifespan in C. elegans. Interestingly, these degenerative symptoms can be attenuated by astragalan treatment. Astragalan is also shown to alleviate oxidative stress through reducing reactive oxygen species level and malondialdehyde content and increasing superoxide dismutase and glutathione peroxidase activities and reduce the expression of proapoptotic gene egl-1 in 6-OHDA-intoxicated nematodes. Further studies reveal that astragalan is capable of elevating the decreased acetylcholinesterase activity induced by 6-OHDA. Together, our results demonstrate that the protective effect of astragalan against 6-OHDA neurotoxicity is likely due to the alleviation of oxidative stress and regulation of apoptosis pathway and cholinergic system and thus provide an important insight into the therapeutic potential of Astragalus polysaccharide in neurodegeneration.

Galactose alters markers of oxidative stress and acetylcholinesterase activity in the cerebrum of rats: protective role of antioxidants

2016 ◽  
Vol 32 (2) ◽  
pp. 359-368 ◽  
Author(s):  
Daniela Delwing-de Lima ◽  
Monique Fröhlich ◽  
Leticia Dalmedico ◽  
Juliana Gruenwaldt Maia Aurélio ◽  
Débora Delwing-Dal Magro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acetylcholinesterase Activity ◽  
Protective Role ◽  
Markers Of Oxidative Stress

Protective Effect of Kaempferol on the Transgenic Drosophila Model of Alzheimer’s Disease

2018 ◽  
Vol 17 (6) ◽  
pp. 421-429 ◽  
Author(s):  
Tanveer Beg ◽  
Smita Jyoti ◽  
Falaq Naz ◽  
Rahul ◽  
Fahad Ali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Neuronal Damage ◽  
Natural Antioxidants ◽  
Acetylcholinesterase Activity ◽  
Model Of Alzheimer’S Disease ◽  
Climbing Ability ◽  
Transgenic Drosophila

Background: Alzheimer’s disease (AD) is characterized by the accumulation and deposition of β-amyloid peptides leading to a progressive neuronal damage and cell loss. Besides several hypotheses for explaining the neurodegenerative mechanisms, oxidative stress has been considered to be one of them. Till date, there is no cure for AD, but the pathogenesis of the disease could be delayed by the use of natural antioxidants. In this context, we decided to study the effect of kaempferol against the transgenic Drosophila expressing human amyloid beta-42. Method: The AD flies were allowed to feed on the diet having 10, 20, 30 and 40µM of kaempferol for 30 days. After 30 days of exposure, the amyloid beta flies were studied for their climbing ability and Aversive Phototaxis Suppression assay. Amyloid beta flies head homogenate was prepared for estimating the oxidative stress markers, Caspase and acetylcholinesterase activity. Results: The results of the present study reveal that the exposure of AD flies to kaempferol delayed the loss of climbing ability, memory, reduced the oxidative stress and acetylcholinesterase activity. Conclusion: Kaempferol could be used as a possible therapeutic agent against the progression of the Alzheimer’s disease.

scholarly journals Cerebral cortex damage induced by acute oral alcohol intake is associated with oxidative stress in Wistar rats (Rattus norvegicus)

2018 ◽  
Vol 7 (1) ◽  
pp. 1113-1120
Author(s):  
Eweoya Olugbenga Olawale ◽  
Ayuba Lolo Shunom ◽  
Ajayi Abayomi
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Wistar Rats ◽  
Alcohol Intake ◽  
Structural Changes ◽  
Sucrose Solution ◽  
Neuronal Loss ◽  
Acetylcholinesterase Activity ◽  
Alcoholic Solution ◽  
Control Group

The prefrontal cortex undergoes functional and structural changes due to binge or chronic alcohol consumption. This study examines alcohol-induced cerebral cortex damage and the association with oxidative stress in an animal model. Twenty-four Wistar rats (12 males and 12 females) weighing 150g to 250g were divided into four groups, A, B, C and D according to their weights. The rats in groups B, C and D were administered with 2mls of 52.5%, 16.5% and 4.3% v/v aqueous alcoholic solution respectively for 21 days. While rats in group A (control group) were given distilled water only, for the same period. The brain of each rat was excised, weighed and fixed in 10% formal saline for histological analysis while others were immersed in ice cold 30% sucrose solution, homogenized and analyzed for superoxide dismutase, malondialdehyde and acetylcholinesterase activity. Results indicate chromatolysis of Nissl bodies, cortical necrosis, and uneven neuronal loss with varying range of vacuolations in the prefrontal cortices of the alcohol treated rats in a dosedependent manner when compared with the control group. Cerebral cortex damage due to acute oral alcohol intake is associated with oxidative stress.Keywords: Brain, cerebral cortex, alcohol, Wistar rats, oxidative stress

scholarly journals Annona atemoya Leaf Extract Improves Scopolamine-Induced Memory Impairment by Preventing Hippocampal Cholinergic Dysfunction and Neuronal Cell Death

2019 ◽  
Vol 20 (14) ◽  
pp. 3538 ◽  
Author(s):  
Eunjin Sohn ◽  
Hye-Sun Lim ◽  
Yu Jin Kim ◽  
Bu-Yeo Kim ◽  
Soo-Jin Jeong
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Passive Avoidance ◽  
Memory Impairment ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Acetylcholinesterase Activity ◽  
Hippocampal Neurogenesis ◽  
Avoidance Task ◽  
Y Maze

We explored the preventative effect of Annona atemoya leaf (AAL) extract on memory impairment in a scopolamine (SCO)-induced cognitive deficit mouse model. Fifty-eight mice were randomly divided into six groups and orally treated with AAL extract at (50, 100, or 200 mg/kg) or tacrine (TAC) for 21 days. Memory deficits were induced by a single injection of 1 mg/kg SCO (i.p.) and memory improvement was evaluated by using behavioral tests such as the passive avoidance task and Y-maze test. The levels of cholinergic functions, neuronal cell death, reactive oxygen species, and protein expression related to hippocampal neurogenesis were examined by immunohistochemical staining and western blotting. The administration of AAL extract improved memory impairment according to increased spontaneous alternation in the Y-maze and step-through latency in passive avoidance test. AAL extract treatment increased the acetylcholine content, choline acetyltransferase, and acetylcholinesterase activity in the hippocampus of SCO-stimulated mice. In addition, AAL extract attenuated oxidative stress-induced neuronal cell death of hippocampal tissue. In terms of the regulatory mechanisms, AAL extract treatment reversed the SCO-induced decreases in the expression of Akt, phosphorylation of cAMP response element binding protein, and brain-derived neurotrophic factor. Our findings demonstrate that AAL extract has the ability to alleviate memory impairment through preventative effect on cholinergic system dysfunction and oxidative stress-related neuronal cell death in a SCO-induced memory deficit animal model. Overall, AAL may be a promising plant resource for the managing memory dysfunction due to neurodegenerative diseases, such as Alzheimer’s disease (AD).

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