Protection against brain tissues oxidative damage as a possible mechanism for improving effects of low doses of estradiol on scopolamine-induced learning and memory impairments in ovariectomized rats

Abstract Background Modulatory effects of soy extract and estradiol on the central nervous system (CNS) have been reported. The effect of soy on scopolamine-induced spatial learning and memory in comparison to the effect of estradiol was investigated. Materials and methods Ovariectomized rats were divided into the following groups: (1) control, (2) scopolamine (Sco), (3) scopolamine-soy 20 (Sco-S 20), (4) scopolamine-soy 60 (Sco-S 60), (5) scopolamine-estradiol 20 (Sco-E 20) and (6) scopolamine-estradiol 60 (Sco-E 60). Soy extract, estradiol and vehicle were administered daily for 6 weeks before training in the Morris water maze (MWM) test. Scopolamine (2 mg/kg) was injected 30 min before training in the MWM test. Results In the MWM, the escape latency and traveled path to find the platform in the Sco group was prolonged compared to the control group (p < 0.001). Treatment by higher doses of soy improved performances of the rats in the MWM (p < 0.05 – p < 0.001). However, treatment with both doses of estradiol (20 and 60 μg/kg) resulted in a statistically significant improvement in the MWM (p < 0.01 – p < 0.001). Cortical, hippocampal and serum levels of malondialdehyde (MDA), as an index of lipid peroxidation, were increased which was prevented by soy extract and estradiol (p < 0.001). Cortical, hippocampal as well as serum levels of the total thiol, superoxide dismutase (SOD) and catalase (CAT) in Sco group were lower than the control group (p < 0.001) while they were enhanced when the animals were treated by soy extract and estradiol (p < 0.01 – p < 0.001). Conclusions It was observed that both soy extract and estradiol prevented learning and memory impairments induced by scopolamine in ovariectomized rats. These effects can be attributed to their protective effects on oxidative damage of the brain tissue.

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The effects of captopril on lipopolysaccharide induced learning and memory impairments and the brain cytokine levels and oxidative damage in rats

Life Sciences ◽

10.1016/j.lfs.2016.10.026 ◽

2016 ◽

Vol 167 ◽

pp. 46-56 ◽

Cited By ~ 22

Author(s):

Azam Abareshi ◽

Mahmoud Hosseini ◽

Farimah Beheshti ◽

Fatemeh Norouzi ◽

Majid Khazaei ◽

...

Keyword(s):

Oxidative Damage ◽

Learning And Memory ◽

Memory Impairments ◽

Cytokine Levels ◽

The Brain

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Effects of PPAR-γ agonist, pioglitazone on brain tissues oxidative damage and learning and memory impairment in juvenile hypothyroid rats

International Journal of Neuroscience ◽

10.1080/00207454.2019.1632843 ◽

2019 ◽

Vol 129 (10) ◽

pp. 1024-1038 ◽

Cited By ~ 2

Author(s):

Yousef Baghcheghi ◽

Hossein Salmani ◽

Farimah Beheshti ◽

Mohammad Naser Shafei ◽

Hamid Reza Sadeghnia ◽

...

Keyword(s):

Oxidative Damage ◽

Learning And Memory ◽

Memory Impairment ◽

Ppar Γ ◽

Brain Tissues

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Involvement of Cholinergic Dysfunction and Oxidative Damage in the Effects of Simulated Weightlessness on Learning and Memory in Rats

BioMed Research International ◽

10.1155/2018/2547532 ◽

2018 ◽

Vol 2018 ◽

pp. 1-11 ◽

Cited By ~ 3

Author(s):

Yongliang Zhang ◽

Qiong Wang ◽

Hailong Chen ◽

Xinmin Liu ◽

Ke Lv ◽

...

Keyword(s):

Oxidative Damage ◽

Learning And Memory ◽

Memory Deficits ◽

Hindlimb Unloading ◽

Sprague Dawley ◽

Negative Effects ◽

Memory Impairments ◽

Cholinergic Dysfunction ◽

Sd Rats ◽

And Oxidative Stress

The present study aimed to determine how the learning and memory gradually change with the prolonged hindlimb unloading (HU) treatment in rats. Different HU durations (7 d, 14 d, 21 d, and 28 d) in Sprague-Dawley (SD) rats were implemented. Cognitive function was assessed using the Morris water maze (MWM) and the shuttle box test. Additionally, parameters about cholinergic activity and oxidative stress were tested. Results showed that longer-than-14 d HU led to the inferior performances in the behavioral tasks. Besides, acetylcholine esterase (AChE) activity, malondialdehyde (MDA) level in brain, reactive oxygen species (ROS), and 8-hydroxy-2-deoxyguanosine (8-OHdG) concentrations of HU rats were significantly increased. Furthermore, choline acetyltransferase (ChAT), superoxide dismutase (SOD), and catalase (CAT) activity in brain were notably attenuated. Most of these effects were more pronounced after longer exposure (21 d and 28 d) to HU, although some indicators had their own characteristics of change. These results indicate that cholinergic dysfunction and oxidative damage were involved in the learning and memory impairments induced by longer-than-14 d HU. Moreover, the negative effects of HU tend to be augmented as the HU duration becomes longer. The results may be helpful to present possible biochemical targets for countermeasures development regarding the memory deficits under extreme environmental conditions.

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Beneficial Effects ofTeucrium poliumand Metformin on Diabetes-Induced Memory Impairments and Brain Tissue Oxidative Damage in Rats

International Journal of Alzheimer s Disease ◽

10.1155/2015/493729 ◽

2015 ◽

Vol 2015 ◽

pp. 1-8 ◽

Cited By ~ 11

Author(s):

S. Mojtaba Mousavi ◽

Saeed Niazmand ◽

Mahmoud Hosseini ◽

Zarha Hassanzadeh ◽

Hamid Reza Sadeghnia ◽

...

Keyword(s):

Oxidative Damage ◽

Lipid Peroxides ◽

Diabetic Group ◽

Control Group ◽

Hydroalcoholic Extract ◽

Memory Impairments ◽

Beneficial Effects ◽

Teucrium Polium ◽

The Brain ◽

Brain Tissues

Objective.The effects of hydroalcoholic extract ofTeucrium poliumand metformin on diabetes-induced memory impairment and brain tissues oxidative damage were investigated.Methods.The rats were divided into: (1) Control, (2) Diabetic, (3) Diabetic-Extract 100 (Dia-Ext 100), (4) Diabetic-Extract 200 (Dia-Ext 200), (5) Diabetic-Extract 400 (Dia-Ext 400), and (6) Diabetic-Metformin (Dia-Met). Groups 3–6 were treated by 100, 200, and 400 mg/kg of the extract or metformin, respectively, for 6 weeks (orally).Results. In passive avoidance test, the latency to enter the dark compartment in Diabetic group was lower than that of Control group (P<0.01). In Dia-Ext 100, Dia-Ext 200, and Dia-Ext 400 and Metformin groups, the latencies were higher than those of Diabetic group (P<0.01). Lipid peroxides levels (reported as malondialdehyde, MDA, concentration) in the brain of Diabetic group were higher than Control (P<0.001). Treatment by all doses of the extract and metformin decreased the MDA concentration (P<0.01).Conclusions.The results of present study showed that metformin and the hydroalcoholic extract ofTeucrium poliumprevent diabetes-induced memory deficits in rats. Protection against brain tissues oxidative damage might have a role in the beneficial effects of the extract and metformin.

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Metformin protects against seizures, learning and memory impairments and oxidative damage induced by pentylenetetrazole-induced kindling in mice

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2014.04.130 ◽

2014 ◽

Vol 448 (4) ◽

pp. 414-417 ◽

Cited By ~ 50

Author(s):

Ran-ran Zhao ◽

Xiao-chen Xu ◽

Fei Xu ◽

Wei-li Zhang ◽

Wen-lin Zhang ◽

...

Keyword(s):

Oxidative Damage ◽

Learning And Memory ◽

Memory Impairments

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Contribution Of Brain Tissue Oxidative Damage In Hypothyroidism-associated Learning and Memory Impairments

Advanced Biomedical Research ◽

10.4103/2277-9175.206699 ◽

2017 ◽

Vol 6 (1) ◽

pp. 59 ◽

Cited By ~ 3

Author(s):

Mahmoud Hosseini ◽

Yousef Baghcheghi ◽

Hossein Salmani ◽

Farimah Beheshti

Keyword(s):

Oxidative Damage ◽

Learning And Memory ◽

Brain Tissue ◽

Memory Impairments

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Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

Ecology and Noospherology ◽

10.15421/032001 ◽

2020 ◽

Vol 31 (1) ◽

pp. 3-10

Author(s):

V. S. Nedzvetsky ◽

V. Ya. Gasso ◽

A. M. Hahut ◽

I. A. Hasso

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Programmed Cell Death ◽

Oxidative Damage ◽

Cadmium Chloride ◽

Glioma Cells ◽

Low Doses ◽

Genotoxic Effects ◽

Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

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