scholarly journals Mitigation of Lead Neurotoxicity by Aqueous Fruit Extract of Adansonia digitata in Adult Wistar Rats

2021 ◽  
pp. 71-82
Author(s):  
Eduitem S. Otong ◽  
Sunday A. Musa ◽  
Barnabas Danborno ◽  
Sohnap J. Sambo
Keyword(s):  
Oxidative Stress ◽  
Brain Damage ◽  
Memory Impairment ◽  
Ache Activity ◽  
Wistar Rats ◽  
Neuronal Degeneration ◽  
Adansonia Digitata ◽  
Male Adult ◽  
Dopamine Concentration ◽  
Group I

Aim: The current study seeks to explore the neuroprotective benefits of Adansonia digitata against lead induced memory impairment, neurotransmitter/AChE activity imbalance, oxidative stress as well as brain damage. Methodology: Thirty male adult rats weighing 160g-200g were divided randomly into six groups (I-V1) consisting of five (5) rats in each group. Group I served as control and were administered with distilled water (1 ml/kg) only while groups II -VI were treatment groups. Group II were administered 250 mg/kg of Adansonia digitata; group III were administered 30 mg/kg of lead; Group IV were administered 250 mg/kg of Adansonia digitata plus 30 mg/kg of lead; Group V were administered 500 mg/kg of Adansonia digitata plus 30 mg/kg of lead; Group VI were administered 30 mg/kg of lead plus 10 mg/kg of succimer. All administrations were carried out through oral gavage for a period of 28 days. Results: Lead administration caused memory impairment, decreased dopamine concentration and AChE activity in brain, induced oxidative stress resulting in brain damage.  Adansonia digitata treatment significantly (P<.001) attenuated memory impairment, modulated dopamine concentration and AChE activity, prevented oxidative stress and ameliorated histopathological changes in the brain of Wistar rats. Conclusion: The result showed that Adansonia digitata ameliorates lead-induced memory impairment in Wistar rats by improving memory index, controlling dopamine concentration and AChE activity, preventing oxidative stress and neuronal degeneration.

scholarly journals The effect of vitamin C on Endosulfan-induced oxidative stress parameters in prepubertal rats

Biomedicine ◽  
2020 ◽  
Vol 39 (2) ◽  
pp. 333-338
Author(s):  
Kalaivani Manokaran ◽  
Vasanthalaxmi Krishnananda Rao ◽  
Nilima . ◽  
Manjula Shimoga Durgoji Rao ◽  
Sucheta Prasanna Kumar
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Wistar Rats ◽  
Statistical Significance ◽  
Treated Group ◽  
Reproductive Organs ◽  
Protective Role ◽  
Control Group ◽  
Group I ◽  
Testicular Weight

Introduction and Aim: Oxidative stress plays a very important role in endosulfan-induced toxic effects on reproductive organs. Vitamin C is a potent antioxidant which plays an important role in decreasing oxidative stress. The present study was aimed to investigate the protective role of vitamin C against endosulfan-induced testicular toxicity in Wistar rats. To investigate a protective effect of vitamin C against endosulfan induced toxicity on biochemical changes. Materials and Methods: Seventy male neonatal Wistar rats were divided into  seven groups. The group  I was taken as the control group, the endosulfan-treated were grouped into II (3 mg/kg body weight (BW) and group III (6 mg/kg BW), Group IV (9 mg/kg BW) and Group V (12 mg/kg BW). Group VI (9 mg/kg BW) and group VII (12 mg/kg BW) were pretreated with vitamin C (20 mg/kg BW) for 60 days. After  the experimental procedures, the testicular weight, lactate dehydrogenase (LDH) enzyme and testosterone in plasma, LDH, steroidogenic enzymes 3?-HSD and 17?-HSD in testis were evaluated. One-way ANOVA was used to determine the statistical significance. Results: Significant improvement in the testicular weight (P<0.05) , LDH (P<0.05) levels both in plasma and testis, increase in testosterone(P<0.001) and steroidogenic enzyme levels(P<0.001) was observed in the group pretreated with vitamin C treated group when compared to the endosulfan treated group. Conclusion: Vitamin C decreases the toxic effect of endosulfan on testis. The present action might be  due to its antioxidative properties.

scholarly journals OXYCAROTENOID LUTEIN REVERSES THE TOXICITY INDUCED BY CARBOFURAN IN WISTAR RATS

2018 ◽  
Vol 10 (7) ◽  
pp. 10
Author(s):  
Binitha P Purushothaman ◽  
Gayathri Valsan ◽  
Ramadasan Kuttan
Keyword(s):  
Oxidative Stress ◽  
Grip Strength ◽  
Wistar Rats ◽  
Pain Threshold ◽  
Strength Test ◽  
Endurance Capacity ◽  
Marker Enzymes ◽  
Threshold Test ◽  
Group I ◽  
Male Wistar Rats

Objective: Elucidation of the protective effect of lutein against carbofuran induced toxicity in Wistar rats.Methods: Male Wistar rats were assigned into 5 groups of five animals. Group I normal received sunflower oil, Group 2 received carbofuran (5 mg/kg b. w.) alone. Group 3-5 received carbofuran plus lutein (50, 100 and 200 mg/kg body weight) respectively. Carbofuran and lutein administration were continued for 14 d. Neurobehavioural markers such as rotarod, grip strength test and pain threshold tests were carried out. After sacrifice, tissues were analysed for marker enzymes, antioxidant enzymes as well as oxidative stress markers.Results: Low dose of carbofuran was found to produce neurobehavioral problems as seen from the decreased retention time during rotarod test, endurance capacity in grip strength test and increased endurance capacity in pain threshold test. They were found to be significantly reversed by oral lutein administration. Administration of lutein restored the decreased acetylcholinesterase produced by carbofuran. Serum and tissue marker enzymes such as lactate dehydrogenase, creatine kinase and gamma-glutamyltransferase, which were increased by carbofuran were decreased by lutein administration. Lutein administration also reduced oxidative stress parameters which were increased by carbofuran.Conclusion: The results showed that carbofuran induced toxicity in male Wistar rats was reversed by carotenoid lutein.

scholarly journals Methyl Gallate Attenuates Doxorubicin-Induced Cardiotoxicity in Rats by Suppressing Oxidative Stress

Scientifica ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Akheruz Zaman Ahmed ◽  
Shakta Mani Satyam ◽  
Prakashchandra Shetty ◽  
Melanie Rose D’Souza
Keyword(s):  
Oxidative Stress ◽  
Normal Control ◽  
Wistar Rats ◽  
Group Iv ◽  
Control Group ◽  
Methyl Gallate ◽  
Group Iii ◽  
Group I ◽  
Female Wistar Rats ◽  
Group Ii

Doxorubicin-induced cardiotoxicity is the leading cause of morbidity and mortality among cancer survivors. The present study was aimed to investigate the cardioprotective potential of methyl gallate; an active polyphenolic nutraceutical, against doxorubicin-induced cardiotoxicity in Wistar rats. Twenty-four female Wistar rats (150–200 g) were divided into four groups (n = 6) which consist of normal control (group I), doxorubicin control (group II), test-A (group III), and test-B (group IV). Group III and group IV animals were prophylactically treated with methyl gallate 150 mg/kg/day and 300 mg/kg/day orally, respectively, for seven days. Doxorubicin (25 mg/kg; single dose) was administered through an intraperitoneal route to group II, III, and IV animals on the seventh day to induce acute cardiotoxicity. On the 8th day, besides ECG analysis, serum CK, CK-MB, LDH, AST, MDA, and GSH were assayed. Following gross examination of isolated hearts, histopathological evaluation was performed by light microscopy. A significant ( p  < 0.05) cardiac injury, as well as oxidative stress, was observed in doxorubicin control rats in comparison to normal control rats. Methyl gallate at both the doses significantly ( p  < 0.05) reduced doxorubicin-induced ECG changes, dyslipidaemia, and elevation of CK, CK-MB, LDH, AST, MDA and increased GSH level. Methyl gallate reversed the doxorubicin-induced histopathological changes in the heart. The present study revealed that methyl gallate exerts cardioprotection against doxorubicin-induced cardiotoxicity in female Wistar rats by suppressing oxidative stress. Our study opens the perspective to clinical studies for consideration of methyl gallate as a potential chemoprotectant nutraceutical in the combination chemotherapy with doxorubicin to limit its cardiotoxicity.

scholarly journals Histological Changes of Wistar Rats' Hippocampus and Entorhinal Cortex After Prenatal Exposure to Mosquito Coil Smoke

2021 ◽  
Vol 1 (1) ◽  
Author(s):  
Shehu K ◽  
Sirajo MU ◽  
Saleh MS
Keyword(s):  
Entorhinal Cortex ◽  
Prenatal Exposure ◽  
Wistar Rats ◽  
Structural Integrity ◽  
Neuronal Degeneration ◽  
Prenatally Exposed ◽  
Mosquito Coil ◽  
Histological Changes ◽  
Group I ◽  
Women And Children

Background: The structural integrity of the hippocampus and the entorhinal cortex appears to be a prerequisite for normal acquisition of information about relational and contextual representation. Increased exposures to pyrethroids by pregnant women and children have raised concerns over their potentials as developmental neurotoxicants. Objectives: We studied the histological changes on the hippocampus and entorhinal cortex of adolescent Wistar rats prenatally exposed to mosquito coil smoke (MCS). Methods: 30 adult Wistar rats (20 females, 10 males) were used for the study. Mating was induced, and pregnancy was confirmed. Pregnant animals were grouped into four, 3 animals per group. Group I was exposed to fresh air. Groups II, III, and IV were exposed to mosquito coil smoke for 4, 6 and 8 hours daily respectively throughout gestation period. On Post-natal day (PND) 29, experimental animals were humanely sacrificed and regions of the hippocampus and entorhinal cortex were processed for histological studies using H & E stain. Results and Conclusion: Our results showed that prenatal exposure to mosquito coil smoke caused neuronal degeneration, distortion in cytoarchitecture of cellular layers and vacuolations in the hippocampus and entorhinal cortex of prenatally exposed groups.

scholarly journals Evaluation of Memory Impairment Following Prenatal Exposure to Mosquito Coil Smoke

2021 ◽  
Vol 1 (1) ◽  
Author(s):  
Shehu K ◽  
Badamosi Im ◽  
Saleh MS
Keyword(s):  
Oxidative Stress ◽  
Entorhinal Cortex ◽  
Prenatal Exposure ◽  
Wistar Rats ◽  
Neurofibrillary Tangle ◽  
Mosquito Coil ◽  
Object Recognition Test ◽  
Animal Group ◽  
Group I ◽  
Significant Impairment

Background: Developmental Neurotoxicity can lead to the buildup of reactive oxygen species which is an indicator to oxidative stress in the prenatally exposed offspring. Neuronal oxidative stress induces neuroinflammation, precedes tangle formation, and disrupts synaptic plasticity. The result of such changes may be expressed into adulthood as behavioral deficits. All together, these mechanisms are implicated in memory disorders. Objectives: To investigate the histochemical changes in the hippocampus and entorhinal cortex of Wistar rats' offspring after prenatal exposure to mosquito coil smoke and its effect on memory. . Methods: 12 pregnant Wistar rats were grouped into four, 3 animals per group. Group I was exposed to fresh air. Groups II, III, and IV were exposed to mosquito coil smoke for 4, 6 and 8 hours daily respectively throughout gestation period. On Post-natal day (PND) 28 and 29, shortterm spatial and recognition memory of adolescent wistar rats were assessed using water licking task and novel object recognition test respectively. For each animal group (I-IV), a total of 8 animals were randomly selected from the litters for neurobehavioral studies. Experimental animals were humanely sacrificed and sections from the hippocampus and entorhinal cortex were processed for histochemical studies using Bielschowsky stain. Data were presented as mean ± SEM; analysed using One-way analysis of variance and Tukey's Multiple Comparison Test (p<0.05). Results and Conclusion: Our results showed significant impairment in short-term recognition and spatial memory of group III and IV adolescent wistar rats when compared with the control (p<0.05) and the formation of neurofibrillary tangle-like structures in neurons of the studied regions. .

scholarly journals The Effect of Intratesticular Injection of Human Adipose-Derived Stem Cell (hADSC) on Testicular Oxidative Stress and Spermatogenesis Process in the Varicocele Rat Model

2021 ◽  
Author(s):  
Safendra Siregar ◽  
Bambang Sasongko Noegroho ◽  
Ricky Adriansjah ◽  
Akhmad Mustafa ◽  
Ananta Bonar
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Wistar Rats ◽  
Histopathological Examination ◽  
Therapy Group ◽  
Intervention Group ◽  
Testicular Tissue ◽  
Control Group ◽  
Group I ◽  
Group Ii

Abstract Introduction: Varicocele is the predominant cause of male infertility and was found in 19% - 41% of men with primary infertility and 45% - 81% of men with secondary infertility. Human adipose Derived Stem Cells (hADSC) can suppress oxidative stress in some oxidative injury model. Therefore, this study would like to investigate the effect of intratesticular hADSC injection on MDA level and spermatogenesis process by histopathological examination in the varicocele rat model.Method: This is an experimental study. A total sampling of 9 male Wistar rats were divided into three groups. Group I consist of 1 Wistar rats without any treatment or model (sham group), group II consist of 4 Wistar rats with varicocele model without hADSC therapy (control group), and group III consist of 4 Wistar rats with varicocele model and were given injections of 1.0x106 hADSC cells intratesticularly 30 days after model was made (therapy group). Testicular tissue was harvested for evaluation. Results: In all varicocele model rats (group II and III), the result of MDA level in therapy group (2.53 mol/liter) was significantly lower than the MDA level in control group (4.43 mol/liter) (p = 0.01). On histopathological examination, the average Johnson's Score in the therapy and control group was 9,77 and 9,18, respectively. The analysis showed Johnson’s score in the intervention group was significantly higher (p = 0.018). Conclusion: Intratesticular injection of hADSC can help reduce MDA levels and improve spermatogenesis process, which is damaged by varicoceles.

scholarly journals Amelioration of Aluminium Chloride (AlCl3) Induced Neurotoxicity by Combination of Rivastigmine and Memantine with Artesunate in Albino Wistar Rats

2019 ◽  
Vol 12 (2) ◽  
pp. 703-711
Author(s):  
S. E. Praveen Kumar ◽  
Kurady Laxminarayana Bairy ◽  
Veena Nayak ◽  
Shiva Kumar Reddy ◽  
Amruth Kiran ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Neuroprotective Effect ◽  
Aluminium Chloride ◽  
Avoidance Task ◽  
Male Adult ◽  
Neuronal Viability ◽  
Combination Treatments ◽  
Age Related ◽  
Group I ◽  
Histopathological Results

Alzheimer’s disease (AD) is an age-related progressive disorder characterized by neurodegeneration and accumulation of abnormal proteins. Artesunate, an anti-malarial drug has recently been shown to have anti-inflammatory, antiviral, angiogenic and other pleiotropic effects. It has also improved cognitive decline induced by hepatic coma which is suggestive of its role in learning and memory. In view of this, the current study was planned to assess the effect of the combination of artesunate with rivastigmine and memantine in aluminium chloride induced neurotoxicity. The study was conducted on 24 male adult albino wistar rats which were divided into four groups (n=6). Group - I to IV received saline, aluminium chloride (AlCl3), AlCl3 + artesunate +rivastigmine, AlCl3 + artesunate + memantine for 60 days respectively. After the 60th day of treatment, all animals were subjected to a passive avoidance task. All the animals were then sacrificed to study the histopathological changes in the hippocampus. Artesunate in combination with rivastigmine and memantine showed significant improvement in memory impairment and reduced neuronal death. Neuronal viability was more prominent in combination treatments as shown by histopathological results. Artesunate in combination with rivastigmine and memantine could be useful in AD. Artesunate can be used as an adjuvant therapy because artesunate combined with standard drugs produced significant neuroprotective effect.

scholarly journals EFFECT OF ECLIPTA ALBA ON SCOPOLAMINE INDUCED AMNESIA IN MICE

2018 ◽  
Vol 8 (5-s) ◽  
pp. 162-168
Author(s):  
Harmel Singh Chahal ◽  
Shailendra Sharma
Keyword(s):  
Oxidative Stress ◽  
Learning And Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Memory Impairment ◽  
Ache Activity ◽  
Memory Deficits ◽  
Eclipta Alba ◽  
Brain Oxidative Stress ◽  
Brain Ache Activity

The present study deals with the evaluation of potential effects of Eclipta alba (EA) in memory impairment of mice. Memory impairment was induced by scopolamine (3 mg/kg, i.p) in animals. To assess learning and memory in mice Morris water maze test was employed. The acetylcholinestrase enzyme (AChE) activity in brain was measured to evaluate the central cholinergic activity. The levels of thiobarbituric acid-reactive species (TBARS) and reduced glutathione (GSH)in brain were estimated to assess the degree of oxidative stress. Scopolamine treatment produces significant impairment of learning and memory in mice, as reflected by a significant decrease in MWM performance. Scopolamine also produced a significant enhancement of brain AChE activity and brain oxidative stress (increase in TBARS and decrease in GSH) levels. EA (300 and 600 mg/kg,oral) significantly prevented scopolamine-induced learning and memory deficits along with decrease of scopolamine-induced rise in brain AChE activity and brain oxidative stress levels. It may be concluded that Eclipta alba has significant protective action against scopolamine induced memory deficits in mice that can be attributed to its anti AChE and anti oxidant actions. Keywords:  Alzheimer disease, Oxidative stress, Morris water Maze, Scopolamine

scholarly journals Effect of sitagliptin on depression in male wistar rats

2019 ◽  
Vol 9 (1) ◽  
pp. 200
Author(s):  
Vidya M. Mahalmani ◽  
Anil P. Hogade ◽  
Sanjay K. Mishra
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Wistar Rats ◽  
Cytokine Gene Expression ◽  
Antidepressant Effect ◽  
Oxidative Stress Markers ◽  
Cytokine Gene ◽  
Stress Markers ◽  
Group I ◽  
Male Wistar Rats

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.

scholarly journals Scopolamine-Induced Memory Impairment in Mice: Neuroprotective Effects of Carissa edulis (Forssk.) Valh (Apocynaceae) Aqueous Extract

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Fanta Sabine Adeline Yadang ◽  
Yvette Nguezeye ◽  
Christelle Wayoue Kom ◽  
Patrick Herve Diboue Betote ◽  
Amina Mamat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Aqueous Extract ◽  
Cholinergic System ◽  
Memory Impairment ◽  
Ache Activity ◽  
Novel Object Recognition ◽  
Novel Object ◽  
Central Cholinergic System

Alzheimer’s disease is first characterised by memory loss related to the central cholinergic system alteration. Available drugs provide symptomatic treatment with known side effects. The present study is aimed to evaluate the properties of Carissa edulis aqueous extract on a Scopolamine mouse model as an attempt to search for new compounds against Alzheimer’s disease-related memory impairment. Memory impairment was induced by administration of 1 mg/kg (i.p.) of Scopolamine for 7 days, and mice were treated with Carissa edulis aqueous extract. Behavioural studies were performed using T-maze and novel object recognition task for assessing learning and memory and open field test for locomotion. Brain acetylcholinesterase enzyme (AChE) activity was measured to evaluate the central cholinergic system. The level of MDA, glutathione, and catalase activity were measured to evaluate the oxidative stress level. Administration of Scopolamine shows a decrease in learning and memory enhancement during behavioural studies. A significant decrease in the time spent in the preferred arm of T-maze, in the time spent in the exploration of the novel object, and in the discrimination index of the familiar object was also observed. The significant impairment of the central cholinergic system was characterised in mice by an increase of AChE activity to 2.55±0.10 mol/min/g with an increase in oxidative stress. Treatment with the different doses of Carissa edulis (62.8, 157, 314, and 628 mg/kg orally administrated) significantly increased the memory of mice in T-maze and novel object recognition tests and also ameliorated locomotion of mice in the open field. Carissa edulis aqueous extract treatment also decreases the AChE activity and brain oxidative stress. It is concluded that administration of Carissa edulis aqueous extract enhances memory of mice by reducing AChE activity and demonstrating antioxidant properties. This could be developed into a novel therapy against memory impairment related to Alzheimer’s disease.

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