scholarly journals HYDROALCOHOLIC EXTRACT OF SWERTIA CHIRATA AND SWERTIA CORDATA ATTENUATES HYPOXIA-MEDIATED MEMORY DYSFUNCTION BY IMPROVING NEURONAL SURVIVAL IN WISTAR RATS

2019 ◽  
pp. 356-362
Author(s):  
KRITIKA KAUSHAL ◽  
HARVINDER SINGH ◽  
ANIL KANT
Keyword(s):  
Oxidative Stress ◽  
Passive Avoidance ◽  
Active Avoidance ◽  
Wistar Rats ◽  
Neuronal Damage ◽  
Memory Dysfunction ◽  
Hydroalcoholic Extract ◽  
Memory Functions ◽  
Swertia Chirata ◽  
The Brain

Objective: Swertia chirata and Swertia cordata have been used in traditional and folk medicines to treat several mental disorders. However, the mechanistic and experimental justification to its traditional use is lacking. The present study was aimed to investigate the neuromodulatory potential of S. chirata and S. cordata during hypoxia-induced neuronal damage in Wistar rats and to determine the underlying mechanism. Methods: Animals were divided into six groups (n=5). Hypoxia was inflicted by subjecting animals to the atmosphere having 10% O2 for 3 days. Animals were administered 100 mg/kg hydroalcoholic extract of S. chirata and S. cordata orally once daily for 7 days, after which motor coordination (Rotarod test) and memory functions (active avoidance test and passive avoidance test) were evaluated. Animals were sacrificed and biochemical investigations for oxidative stress and histopathology were performed. Results: Subjecting animals to hypoxia resulted in marked memory dysfunction, and extract treatments improved memory functions in active avoidance and passive avoidance task. Hypoxiainduced the marked oxidative stress as indicated by the significantly elevated reactive oxygen species and lipid peroxidation and depleted catalase and glutathione levels in the hippocampus. S. chirata and S. cordata treatment alleviated oxidative stress in the hippocampus region of the brain. Brain histopathology confirmed that hypoxia resulted in significant neuronal damage and extract treatment efficiently rescued neurons from hypoxic damage. Overall, S. chirata extract treatment was observed to have better neuromodulatory effect than S. cordata during hypoxia. Conclusion: Hypoxia induced memory dysfunction by inflicting neuronal damage and oxidative stress in the hippocampus region of the brain. The hydroalcoholic extract of S. chirata and S. cordata improved memory functions in hypoxic animals by alleviating hippocampal oxidative stress and by improving neuronal morphology and survival.

scholarly journals ANTIOXIDANT AND HEPATOPROTECTIVE EFFECT OF SWERTIA CHIRATA ON HYPOXIA-INDUCED OXIDATIVE STRESS IN WISTAR RATS

2019 ◽  
Vol 12 (1) ◽  
pp. 76
Author(s):  
Kritika Kaushal ◽  
Harvinder Singh ◽  
Anil Kant Thakur
Keyword(s):  
Oxidative Stress ◽  
Liver Function ◽  
Wistar Rats ◽  
Hepatic Damage ◽  
Ros Generation ◽  
Dependent Manner ◽  
Traditional Use ◽  
Hydroalcoholic Extract ◽  
Swertia Chirata ◽  
Liver Functions

Objective: Swertia chirata has been used in traditional and folklore medicine to treat several ailments such as hepatic disorders. However, the mechanistic and experimental justification to its traditional use is lacking. The present study was aimed to investigate the hepatoprotective potential of S. chirata during hypoxia (HYP)-induced hepatic damage in Wistar rats and to determine the underlying mechanism.Methods: Hydroalcoholic extract of S. chirata was prepared using Soxhlet extraction. Animals were divided into six groups (n=5). Animals in the HYP groups were subjected to HYP for 3 days (10% O2) to induce oxidative stress and hepatic damage. 50 and 100 mg/kg extract treatments were provided orally once daily for 7 days after which animals were sacrificed, and biochemical investigations for oxidative stress, liver function tests, and hepatic histopathology were performed.Results: HYP-induced marked oxidative stress as indicated by the significantly elevated mitochondrial ROS generation, lipid peroxidation, glutathione, and depleted catalase levels. Liver function test indicated hepatic damage as the levels of serum glutamic-oxaloacetic transaminase, serum glutamic pyruvic transaminase, and aspartate transaminase were significantly elevated in HYP animals. S. chirata treatment alleviated oxidative stress and improved liver functions in a dose-dependent manner. Liver histopathology confirmed the marked hepatic damage induced by HYP and revealed that S. chirata efficiently rescued liver from hypoxic damage.Conclusion: Hydroalcoholic extract of S. chirata is a potent hepatoprotective intervention which was associated with its potential to alleviate oxidative stress and improve liver functions. Moreover, it could find clinical application as a safer and alternative remedy for liver ailments.

scholarly journals Riboceine Regimen Attenuates Ethanol-induced Neuronal Damage in the Cerebellum of Adult Male Wistar Rats

2021 ◽  
Vol 15 (4) ◽  
pp. 249-256
Author(s):  
Taiwo Adekemi Abayomi ◽  
◽  
Olorunfemi Samuel Tokunbo ◽  
Moyinoluwa Ajayi ◽  
Olawale Ayobami Abayomi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Neuronal Damage ◽  
Motor Impairment ◽  
Stress Profile ◽  
Stress Markers ◽  
Ethanol Toxicity ◽  
Male Wistar Rats ◽  
Cerebellar Astrocytes ◽  
The Brain

Background: Although ethanol exerts its neurotoxic effect on the brain through inflammatory and oxidative processes, the effect of Riboceine on the brain following ethanol neurotoxicity is yet to be elucidated. Therefore, this study was designed to evaluate the effects of riboceine on the cellular, behavioral, and molecular impairments induced by ethanol toxicity in rats. Methods: A total of 24 male Wistar rats weighing between 160-170 grams were used for the study, and were divided into four groups of six rats each. After completion of the administration of ethanol and riboceine, and testing for motor impairment, the rats were sacrificed. The cerebellum was excised and processed for oxidative stress analyses, based on oxidative stress markers and histological examinations. The immunohistochemical expression of astrocytes in the cerebellum was examined, using Glial Fibrillary Acidic Protein (GFAP) stain. Results: This study demonstrated that ethanol-induced neurotoxicity in the cerebellum, characterized by increased oxidative stress profile, astrocyte activation, and neuronal death in the cerebellum, especially the Purkinje layer. Necrosis, significant decrease in Superoxide Dismutase (SOD), Catalase (CAT) and Gluathione (GSH) activities (P<0.05) as well as astrogliosis was associated with ethanol treatment. However, riboceine was observed to significantly increase the cerebellar SOD, CAT and GSH activities with significantly reduced Malondialdehyde (MDA) levels (P<0.05). It also attenuated the histomorphological alteration of the cerebellum and reduced the cerebellar astrocytes activation following ethanol-induced neurotoxicity, thus leading to the attenuation of motor impairment. Conclusion: Riboceine attenuated motor impairment caused by chronic ethanol-induced neurotoxicity, suggestive of its anti-oxidative and anti-inflammatory properties.

scholarly journals ANTIOXIDANT AND HEPATOPROTECTIVE EFFECT OF SWERTIA CHIRATA ON HYPOXIA-INDUCED OXIDATIVE STRESS IN WISTAR RATS

2019 ◽  
Vol 12 (1) ◽  
pp. 76
Author(s):  
Kritika Kaushal ◽  
Harvinder Singh ◽  
Anil Kant Thakur
Keyword(s):  
Oxidative Stress ◽  
Liver Function ◽  
Wistar Rats ◽  
Hepatic Damage ◽  
Ros Generation ◽  
Dependent Manner ◽  
Traditional Use ◽  
Hydroalcoholic Extract ◽  
Swertia Chirata ◽  
Liver Functions

Objective: Swertia chirata has been used in traditional and folklore medicine to treat several ailments such as hepatic disorders. However, the mechanistic and experimental justification to its traditional use is lacking. The present study was aimed to investigate the hepatoprotective potential of S. chirata during hypoxia (HYP)-induced hepatic damage in Wistar rats and to determine the underlying mechanism.Methods: Hydroalcoholic extract of S. chirata was prepared using Soxhlet extraction. Animals were divided into six groups (n=5). Animals in the HYP groups were subjected to HYP for 3 days (10% O2) to induce oxidative stress and hepatic damage. 50 and 100 mg/kg extract treatments were provided orally once daily for 7 days after which animals were sacrificed, and biochemical investigations for oxidative stress, liver function tests, and hepatic histopathology were performed.Results: HYP-induced marked oxidative stress as indicated by the significantly elevated mitochondrial ROS generation, lipid peroxidation, glutathione, and depleted catalase levels. Liver function test indicated hepatic damage as the levels of serum glutamic-oxaloacetic transaminase, serum glutamic pyruvic transaminase, and aspartate transaminase were significantly elevated in HYP animals. S. chirata treatment alleviated oxidative stress and improved liver functions in a dose-dependent manner. Liver histopathology confirmed the marked hepatic damage induced by HYP and revealed that S. chirata efficiently rescued liver from hypoxic damage.Conclusion: Hydroalcoholic extract of S. chirata is a potent hepatoprotective intervention which was associated with its potential to alleviate oxidative stress and improve liver functions. Moreover, it could find clinical application as a safer and alternative remedy for liver ailments.

scholarly journals Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 229
Author(s):  
JunHyuk Woo ◽  
Hyesun Cho ◽  
YunHee Seol ◽  
Soon Ho Kim ◽  
Chanhyeok Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Computational Models ◽  
Neuronal Damage ◽  
Living Organism ◽  
The Body ◽  
Mitochondrial Functions ◽  
A Cell ◽  
The Brain ◽  
And Oxidative Stress

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5′-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

scholarly journals Neuroprotective Effect of Antioxidants in the Brain

2020 ◽  
Vol 21 (19) ◽  
pp. 7152 ◽  
Author(s):  
Kyung Hee Lee ◽  
Myeounghoon Cha ◽  
Bae Hwan Lee
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Intracellular Signaling ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
High Energy ◽  
Antioxidant Compounds ◽  
The Brain

The brain is vulnerable to excessive oxidative insults because of its abundant lipid content, high energy requirements, and weak antioxidant capacity. Reactive oxygen species (ROS) increase susceptibility to neuronal damage and functional deficits, via oxidative changes in the brain in neurodegenerative diseases. Overabundance and abnormal levels of ROS and/or overload of metals are regulated by cellular defense mechanisms, intracellular signaling, and physiological functions of antioxidants in the brain. Single and/or complex antioxidant compounds targeting oxidative stress, redox metals, and neuronal cell death have been evaluated in multiple preclinical and clinical trials as a complementary therapeutic strategy for combating oxidative stress associated with neurodegenerative diseases. Herein, we present a general analysis and overview of various antioxidants and suggest potential courses of antioxidant treatments for the neuroprotection of the brain from oxidative injury. This review focuses on enzymatic and non-enzymatic antioxidant mechanisms in the brain and examines the relative advantages and methodological concerns when assessing antioxidant compounds for the treatment of neurodegenerative disorders.

P3-073: NAD+ metabolism, and oxidative stress in the brain of aging Wistar rats: Is there a link?

2012 ◽  
Vol 8 (4S_Part_13) ◽  
pp. P478-P478
Author(s):  
Nady Braidy ◽  
Anne Poljak ◽  
Tharusha Jayasena ◽  
Gilles Guillemin ◽  
George Smythe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Nad Metabolism ◽  
The Brain ◽  
And Oxidative Stress

Anxiety-related behavior in hyperhomocysteinemia induced by methionine nutritional overload in rats: role of the brain oxidative stress

2016 ◽  
Vol 94 (10) ◽  
pp. 1074-1082 ◽  
Author(s):  
Dragan Hrncic ◽  
Jelena Mikić ◽  
Aleksandra Rasic-Markovic ◽  
Milica Velimirović ◽  
Tihomir Stojković ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Open Field ◽  
Wistar Rats ◽  
Brain Regions ◽  
Oxidative Status ◽  
Standard Diet ◽  
Male Wistar Rats ◽  
Brain Oxidative Stress ◽  
The Brain

The aim of this study was to examine the effects of a methionine-enriched diet on anxiety-related behavior in rats and to determine the role of the brain oxidative status in these alterations. Adult male Wistar rats were fed from the 30th to 60th postnatal day with standard or methionine-enriched diet (double content comparing with standard diet: 7.7 g/kg). Rats were tested in open field and light–dark tests and afterwards oxidative status in the different brain regions were determined. Hyperhomocysteinemia induced by methionine-enriched diet in this study decreased the number of rearings, as well as the time that these animals spent in the center of the open field, but increased index of thigmotaxy. Oxidative status was selectively altered in the examined regions. Lipid peroxidation was significantly increased in the cortex and nc. caudatus of rats developing hyperhomocysteinemia, but unaltered in the hippocampus and thalamus. Based on the results of this research, it could be concluded that hyperhomocysteinemia induced by methionine nutritional overload increased anxiety-related behavior in rats. These proanxiogenic effects could be, at least in part, a consequence of oxidative stress in the rat brain.

Differential oxidative stress and DNA damage in rat brain regions and blood following chronic arsenic exposure

2008 ◽  
Vol 24 (4) ◽  
pp. 247-256 ◽  
Author(s):  
D Mishra ◽  
SJS Flora
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Drinking Water ◽  
Wistar Rats ◽  
Arsenic Exposure ◽  
Brain Regions ◽  
Single Strand ◽  
Male Wistar Rats ◽  
Chronic Arsenic Exposure ◽  
The Brain

Chronic arsenic poisoning caused by contaminated drinking water is a wide spread and worldwide problem particularly in India and Bangladesh. One of the possible mechanisms suggested for arsenic toxicity is the generation of reactive oxygen species (ROS). The present study was planned 1) to evaluate if chronic exposure to arsenic leads to oxidative stress in blood and brain – parts of male Wistar rats and 2) to evaluate which brain region of the exposed animals was more sensitive to oxidative injury. Male Wistar rats were exposed to arsenic (50 ppm sodium arsenite in drinking water) for 10 months. The brain was dissected into five major parts, pons medulla, corpus striatum, cortex, hippocampus, and cerebellum. A number of biochemical variables indicative of oxidative stress were studied in blood and different brain regions. Single-strand DNA damage using comet assay was also assessed in lymphocytes. We observed a significant increase in blood and brain ROS levels accompanied by the depletion of GSH/GSSG ratio and glucose-6-phosphate dehydrogenase (G6PD) activity in different brain regions of arsenic-exposed rats. Chronic arsenic exposure also caused significant single-strand DNA damage in lymphocytes as depicted by comet with a tail in arsenic-exposed cells compared with the control cells. On the basis of results, we concluded that the cortex region of the brain was more sensitive to oxidative injury compared with the other regions studied. The present study, thus, leads us to suggest that arsenic induces differential oxidative stress in brain regions with cortex followed by hippocampus and causes single-strand DNA damage in lymphocytes.

scholarly journals The Effect of a Traditional Preparation Containing Piper nigrum L. and Bunium persicum (Boiss.) B.Fedtsch. on Immobility Stress-Induced Memory Loss in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Marzieh Rashedinia ◽  
Mina Mojarad ◽  
Forouzan Khodaei ◽  
Ali Sahragard ◽  
Mohammad Javad Khoshnoud ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Motor Coordination ◽  
Black Pepper ◽  
Aqueous Extracts ◽  
Memory And Learning ◽  
Hydroalcoholic Extract ◽  
The Brain ◽  
And Oxidative Stress

Objective. Alzheimer’s disease is a progressive, age-related, and neurodegenerative disease characterized by mental decline. The exact cause of Alzheimer’s disease is unclear, but cholinergic dysfunction, protein accumulation, and oxidative stress are among the most important hypotheses. The main purpose of our study was to investigate the effects of aqueous and hydroalcoholic extract combination of these two medicinal plants, black pepper and cumin (as a related formulation in traditional Persian medicine), on memory and learning of an immobilized stress animal model. Methods. In this study, hydroalcoholic and aqueous extracts of cumin and black pepper fruits were prepared. Six groups of mice were treated orally for 2 weeks: control group, immobility stress, and stress-induced immobility mice received different doses of the hydroalcoholic extract (100 and 200 mg/kg) and aqueous extract (100 and 200 mg/kg). The shuttle box, novel object detection, and rotarod test were used to evaluate memory and learning. The activities of acetylcholinesterase, catalase (CAT), and superoxide dismutase (SOD) and the level of reduced glutathione (GSH) and malondialdehyde (MDA) were measured in the brain tissue. Results. Immobility stress significantly reduced learning and motor coordination. Furthermore, MDA levels and acetylcholinesterase activity were significantly increased, while CAT and SOD activities were significantly reduced in the brain of immobility-induced stress mice. Other findings indicated that hydroalcoholic and aqueous extracts (100 and 200 mg/kg) of cumin and black pepper fruits have an improving effect on animal motor coordination and learning ability, GSH content, and CAT, SOD, and acetylcholinesterase enzyme function in comparison with stress groups ( p < 0.05 ). Conclusion. The hydroalcoholic and aqueous extracts of cumin and black pepper fruits have protective effects against stress-induced memory deficit and oxidative stress and may have beneficial therapeutic effect in the treatment of neurodegenerative diseases.

scholarly journals Walnut Protein Hydrolysates Play a Protective Role on Neurotoxicity Induced by d-Galactose and Aluminum Chloride in Mice

Molecules ◽  
2018 ◽  
Vol 23 (9) ◽  
pp. 2308 ◽  
Author(s):  
Li Feng ◽  
Xiaojing Wang ◽  
Fei Peng ◽  
Jianqiao Liao ◽  
Yifan Nai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Aluminum Chloride ◽  
Neuroprotective Effect ◽  
Protective Role ◽  
Protein Hydrolysates ◽  
Memory Functions ◽  
Cholinergic Dysfunction ◽  
Meal Protein ◽  
The Brain

In recent years, with an increase in the aging population, neurodegenerative diseases have attracted more and more attention. This study aimed to investigate the potential neuroprotective effect of defatted walnut meal protein hydrolysates (DWMPH) on neurotoxicity induced by d-galactose (d-gal) and aluminum chloride (AlCl3) in mice. The animal models were established by combining treatments with d-gal (200 mg/kg/day, subcutaneously) and AlCl3 (100 mg/kg in drinking water) for 90 days. During the 90 days, 1 g/kg of DWMPH was administrated orally every day. The results indicated that DWMPH treatment alleviated oxidative stress, reversed cholinergic dysfunction, and suppressed the release of proinflammatory cytokines in the brains of d-gal + AlCl3-treated mice, and thus improving the learning and memory functions of these mice, which was closely correlated with the strong antioxidant activity of DWMPH. This finding suggests that DWMPH might be a promising dietary supplement in improving neuronal dysfunctions of the brain.

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