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 ◽  
...  

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.

2014 ◽  
Vol 66 (3) ◽  
pp. 1075-1081
Author(s):  
Ivan Simic ◽  
Violeta Iric-Cupic ◽  
Rada Vucic ◽  
Marina Petrovic ◽  
Violeta Mladenovic ◽  
...  

The aim of the present study was to evaluate the subchronic effects of 3,4-methylenedioxymethamphetamine on several oxidative stress markers: index of lipid peroxidation (ILP), superoxide dismutase (SOD) activity, superoxide radical (O2.-) levels, and reduced glutathione (GSH) levels in the frontal cortex, striatum and hippocampus of the rat. The study included 64 male Wistar rats (200-250g). The animals were treated per os with of 5, 10, or 20 mg/kg of 3,4-methylenedioxymethamphetamine (MDMA) every day for 15 days. The subchronic administration of MDMA resulted in an increase in ILP, SOD and O2.-, and a decrease in GSH, from which we conclude that oxidative stress was induced in rat brain.


2016 ◽  
Vol 94 (10) ◽  
pp. 1074-1082 ◽  
Author(s):  
Dragan Hrncic ◽  
Jelena Mikić ◽  
Aleksandra Rasic-Markovic ◽  
Milica Velimirović ◽  
Tihomir Stojković ◽  
...  

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.


2008 ◽  
Vol 24 (4) ◽  
pp. 247-256 ◽  
Author(s):  
D Mishra ◽  
SJS Flora

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.


Author(s):  
Vidya M. Mahalmani ◽  
Anil P. Hogade ◽  
Sanjay K. Mishra

Background: Growing evidence supports relationship between depression and inflammation. The hypothesis of involvement of inflammatory pathways in depression is supported by the findings of increased levels of proinflammatory cytokines. So, we decided to evaluate the effect of sitagliptin on depression using forced swim test (FST) and possible effects of sitagliptin on serum oxidative stress markers and cytokine gene expression in rat hippocampus.Methods: FST model was used to evaluate antidepressant effect in male wistar rats. Rats in group I (control group) were given normal saline, group II (standard group) were given fluoxetine, group III and IV (test groups) were given sitagliptin 5 mg/kg and sitagliptin 9 mg/kg respectively. All the drugs in all groups were given per orally. At the end, animals were sacrificed and blood was collected. Hippocampus of rat brain was dissected out. Serum oxidative stress markers and hippocampal pro inflammatory cytokine gene expression analysis was carried out.Results: Sitagliptin 5 mg/kg and 9 mg/kg showed reduction in depressive symptoms and hippocampal cytokine gene expression in comparison to control. In case of serum oxidative stress markers, there was statistically significant reduction in nitric oxide levels with stagliptin 9 mg/kg. Although there was a decrease in the levels of catalase and increase in the levels of glutathione with standard and test groups, the results were not statistically significant.Conclusions: The present study showed significant antidepressant effect activity of standard and test groups. Hence, further research should be carried out to substantiate above results.


Author(s):  
KRITIKA KAUSHAL ◽  
HARVINDER SINGH ◽  
ANIL KANT

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.


Author(s):  
Ijeoma Ezebuiro ◽  
Chibuike Obiandu ◽  
Friday Saronee ◽  
Adesua C. Obiandu

Introduction: Cnidoscolus aconitifolius is considered to be an important and effective medicinal plant in folklore remedies where it has been applied as an alternative therapy for the treatment of various ailments. Aim: The present study aims to determine the effects of Cnidoscolus aconitifolius on lipid profile and some oxidative stress markers of male Wistar rats. Methodology: A total of 15 male wistar rats were procured for the study and randomly assigned into three groups of 5 rats each. Group 1 served as control and received distilled water only. Group 2 received 200 mg/kg and group 3 received 400mg/kg of the hydromethanolic (1:4) extract of Cnidoscolus aconitifolius which was administered as single daily dose using oral cannula. On completion of treatment, blood samples were collected by cardiac puncture for determination of some serum lipid parameters and oxidative stress markers. Results: Results showed that there were no significant difference in the serum level of total cholesterol, triglyceride, low density lipoprotein cholesterol and high density lipoprotein cholesterol at both doses of the extract, compared to control. However, compared to control, there was a significant (p<0.05) increase in the activity of superoxide dismutase and glutathione reductase but significant reduction in malondialdehyde level. The catalase enzyme activity was not significant. Conclusion: The result obtained suggest that the extract may be useful in reducing oxidative stress by improving some antioxidant enzyme activities and may also prevent cell death due to lipid peroxidation.


Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 229
Author(s):  
JunHyuk Woo ◽  
Hyesun Cho ◽  
YunHee Seol ◽  
Soon Ho Kim ◽  
Chanhyeok Park ◽  
...  

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.


Life Sciences ◽  
2006 ◽  
Vol 79 (23) ◽  
pp. 2187-2193 ◽  
Author(s):  
Maria H.V.M. Jacob ◽  
Mauro R.N. Pontes ◽  
Alex S.R. Araújo ◽  
Jaqueline Barp ◽  
Maria C. Irigoyen ◽  
...  

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