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 Apoptotic Inducement of Neuronal Cells by Aluminium Chloride and the Neuroprotective Effect of Eugenol in Wistar Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Samuel Bolaji Mesole ◽  
Okpanachi Omachonu Alfred ◽  
Uthman Ademola Yusuf ◽  
Lwiindi Lukubi ◽  
Dailesi Ndhlovu
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Wistar Rats ◽  
Caspase 3 ◽  
Anaesthetic Agent ◽  
Neuroprotective Effect ◽  
Aluminium Chloride ◽  
Neuroprotective Effects ◽  
Stress Markers ◽  
Bax Protein

Aluminium is known to accelerate oxidative stress, amyloid beta (Aβ) deposition, and plaque formation in the brain of rats. Objective. The present study is aimed at studying the neuroprotective effects of eugenol following aluminium-induced neurotoxicity on caspase-3, apoptotic proteins (Bcl-2 and Bax), and oxidative stress markers in Wistar rats such as superoxide dismutase (SOD), glutathione peroxidase (GPx), nitric oxide (NO), and assay oxidative stress to mitochondrial DNA (mtDNA) by measuring the levels of 8-hydroxy-2-deoxyguanosine (8-OHdG). Materials and methods. Twenty (20) adult Wistar rats were randomly divided into four (4) groups with five animals in each group. Route of administration was oral throughout the duration of this study and this study lasted for 21 days. Rats were sacrificed 24 hours after administration of the last dose (i.e., day 22) with 0.8 mg/kg ketamine as an anaesthetic agent. Results. Exposure to AlCl3 resulted in a significant (p<0.01) elevation in the levels of nitric oxide and 8-hydroxy-2-deoxyguanosine (8-OHdG), enhanced the activity of caspase-3, increased the level of proapoptotic protein Bax and reduced the levels of antiapoptotic protein Bcl-2, and significantly (p<0.01) reduced the levels of SOD and GPx. However, treatment with eugenol resulted in a significant reduction (p<0.01) in the levels of nitric oxide (NO) and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, inhibited the activity of caspase-3, increased levels of Bcl-2 and significantly (p<0.05) reduced levels of Bax protein, respectively, and also significantly (p<0.05) increased the levels of SOD and GPx. Our results would hereby suggest that eugenol would provide a therapeutic value against aluminium-induced oxidative stress as related to antioxidant and antiapoptotic activities.

scholarly journals Erratum to: Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

2015 ◽  
Vol 40 (9) ◽  
pp. 2006-2006 ◽  
Author(s):  
Arokiasamy Justin Thenmozhi ◽  
Tharsius Raja William Raja ◽  
Udaiyappan Janakiraman ◽  
Thamilarasan Manivasagam
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Wistar Rats ◽  
Neuroprotective Effect ◽  
Aluminium Chloride

scholarly journals Effects of Aluminium Chloride Exposure on the Histology of the Cerebral Cortex of Adult Wistar Rats

2012 ◽  
Vol 3 (1) ◽  
Author(s):  
Adebayo Adekunle Buraimoh ◽  
Samuel Adeniyi Ojo ◽  
Joseph Olajide Hambolu ◽  
Sunday Samuel Adebisi
Keyword(s):  
Cerebral Cortex ◽  
Wistar Rats ◽  
Group Iv ◽  
Aluminium Chloride ◽  
Mammalian Brain ◽  
Control Group ◽  
Perceptual Awareness ◽  
Group V ◽  
Group Iii ◽  
Group I

Aluminium (Al) is presents in many manufactured foods, medicines and is also added to drinking water for purification purposes. Human exposure to Al has been increasing over the last decades. Al exposure and neurological impairments demonstrate mixed findings. The cerebral cortex is a sheet of neural tissue that is outer-most to the cerebrum of the mammalian brain and it plays a key role in memory, attention, perceptual awareness, thought, language, and consciousness.The objectives of this study was to investigate the possible effects that aluminium Chloride could have on the histology of cerebral cortex. Total of twenty adult wistar rats were used for this experiment. The wistar rats were divided into five groups; group I was the control, group II received 475mg/Kg, group III received 950mg/kg, group IV received 1,425mg/kg and group V received 1,900mg/kg via oral intubation for a duration of Eight weeks. The wistar rats were humanly sacrificed and the brain was removed and immediately fixed in bouin fluid. The histological observations of the aluminium treated groups revealed extensive neuronal vacuolation and necrosis (neuro-degeneration) of the cerebral cortex of wistar rats.Based on our observations, we therefore conclude that Aluminium chloride exposure has neurodegenerative effects on the histology of cerebral cortex of adult wistar rats especially at higher dose. Therefore, caution should be taken in its usage.

scholarly journals Zinc Phosphide-Induced Hepato-Nephrotoxicity in Wistar Rats: The Ameliorative Role of Curcumin from Curcuma longa Rhizome

2021 ◽  
pp. 1-8
Author(s):  
Kemi F. Akinwunmi ◽  
Emmanuel B. Ofeniforo ◽  
Kehinde H. Fasunle
Keyword(s):  
Body Weight ◽  
Wistar Rats ◽  
Corn Oil ◽  
Curcuma Longa ◽  
Saline Group ◽  
Zinc Phosphide ◽  
Time Interval ◽  
Male Adult ◽  
Experimental Animals ◽  
Group I

Globally used pesticides contains zinc phosphide (ZnP) which are toxic. This present study was carried out to investigate the potency of bioactive curcumin in ameliorating the toxicity of zinc phosphide on biochemical enzymes present in kidney and liver of Wistar rats. A total of 30 (120–150 g) male adult Wistar rats were used. Experimental animals were divided into five groups and treated as follows for a period of 21 days: Group I rats, serving as the control, orally received 1 ml/kg body weight of corn oil with administration of same volume of saline. Group II rats were orally administered Zinc phosphide at a dose of 4.57 mg/kg body weight (one-tenth LD50) in corn oil. Group III rats orally received curcumin at a dose of 100 mg/kg body weight. Groups IV and V rats were orally administered curcumin at graded doses of 100 and 200 mg/kg body weight respectively, 2 hours before administration of Zinc phosphide. At the end of the time interval, experimental animals were anesthesized with diethylether and organs (kidney and liver) were harvested for biochemical assays. The oral administration of Zinc phosphide at 4.57 mg/kg body weight for 21 days resulted in a significant increase in hepatic and nephridial malondialdehyde. This index of lipid peroxidation, was accompanied by decreased activity of the antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) followed by a drastic reduction in the non-enzymatic antioxidant indices of reduced glutathione when compared to control. Pre-administration of Curcumin significantly ameliorated zinc phosphide-induced hepatic and nephrotic effects by subduing oxidative stress indices and improving antioxidant status. The result of the present study shows that curcumin has a protective effect against zinc phosphide induced liver and kidney damage in male Wistar rats.

Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

2015 ◽  
Vol 40 (4) ◽  
pp. 767-776 ◽  
Author(s):  
Arokiasamy Justin Thenmozhi ◽  
Tharsius Raja William Raja ◽  
Udaiyappan Janakiraman ◽  
Thamilarasan Manivasagam
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Wistar Rats ◽  
Neuroprotective Effect ◽  
Aluminium Chloride

scholarly journals Health Status of Male Adult Wistar Rats from Two Experimental Animal Houses of UFMG: Leukocyte Counts, Feces and Lung Histological Exams

2002 ◽  
Vol 45 (3) ◽  
pp. 287-291
Author(s):  
Bruno Horta Andrade ◽  
Miriam Martins Chaves ◽  
Angela Maria Ribeiro
Keyword(s):  
Health Status ◽  
Experimental Animal ◽  
Behavior Modification ◽  
Wistar Rats ◽  
Histological Study ◽  
Clinical Signs ◽  
Male Adult ◽  
Group I ◽  
Leukocyte Counts ◽  
Group Ii

A study was conducted to compare health status of male adult Wistar rats from two Experimental Animal Houses of UFMG with literature data of SPF (free from specific pathogens) and conventional rats. The animals were divided into two groups: Group I (n=10), rats from the experimental animal houses of FAFICH and Group II (n=10) from ICB and following aspects were studied: a) evident clinical signs (behavior modification, hair loss (alopecia), b) leukocyte counts, c) feces exam and d) histological study of the lungs. The rats did not show clinical signs. However, when compared with SPF and conventional rats, both the groups showed a significant increase (p<0,05) of leukocyte count. On feces exam we detected some parasites and on lung histological exam we observed fungus (Group I) and bacteria (Group II). These results showed that the health status of the rats was not satisfactory and required improvements in the conditions of the animal houses.

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 Neuroprotective Effect of Carvedilol on Diabetic Neuropathy: An In Vitro Study

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Rania M. Magadmi ◽  
Mujahid A. Alsulaimani ◽  
Aziza Rashed Al-Rafiah ◽  
Ahmed Esmat
Keyword(s):  
Diabetic Neuropathy ◽  
In Vitro Model ◽  
Neuroprotective Effect ◽  
Neuronal Morphology ◽  
Diabetic Patients ◽  
Activating Transcription Factor 3 ◽  
Male Adult ◽  
Neuronal Viability ◽  
Vitro Model

Diabetic neuropathy serves as a major complication for diabetic patients across the world. The use of effective treatment is integral for reducing the health complications for diabetic patients. This study has evaluated the carvedilol potential neuroprotective effect on diabetic neuropathy. An in vitro model of diabetic neuropathy was used, including dorsal root ganglia (DRG) that were cultured from male adult mice C57BL. These were incubated for about twenty-four hours in high glucose (HG) media (45 mM). Some cells were incubated with carvedilol (10 μM). Neuronal viability, neuronal morphology, and activating transcription factor 3 (AFT3) were measured. The cell viability was decreased, along with neuronal length, soma area, and soma perimeter with HG media. Also, there was an overexpression of ATF3, which is a neuronal stress response marker. The pretreatment with carvedilol increased the viability of DRG as compared to HG-treated cells. Also, it significantly protected the DRG from HG-induced morphology changes. Though it shows a decrease in AFT3 expression, the statistical results were insignificant. The current study demonstrates the neuroprotective effect of carvedilol against HG-induced DN using an in vitro model. This could be through carvedilol antioxidant effects.

Renal Cortical Slices: An In Vitro Model for Kidney Metabolism and Toxicity

1992 ◽  
Vol 20 (1) ◽  
pp. 71-76
Author(s):  
Andrea Trevisan ◽  
Stefano Maso ◽  
Paola Meneghetti
Keyword(s):  
Wistar Rats ◽  
Reduced Glutathione ◽  
Organic Anion ◽  
Cortical Slice ◽  
Lactate Dehydrogenase Release ◽  
Age Related ◽  
Renal Cortical Slice ◽  
Male Wistar Rats ◽  
Vitro Model

The in vitro renal cortical slice model was used to study: 1) the effects on the kidney of some haloalkanes and haloalkenes using 3-month-old male Wistar rats; 2) influence of age and sex on renal cortical slice indices in non-treated rats; and 3) effects of 1,2-dichloropropane on the slices after pretreatment of 3-month-old male Wistar rats with DL-butathionine-[S,R]-sulphoximine. The most nephrotoxic chemical used was 1,3-dichloropropene, which caused a total depletion in the levels of reduced glutathione, a high peroxidation of lipid (about three thousand-fold with respect to control), a significant release of tubular enzymes into the medium, and loss of organic anion ( p-aminohippurate) accumulation. All the chemicals affected the cytosol more than the brush border. The most remarkable age-related differences in the untreated slices were the progressive decrease of reduced glutathione (p<0.05 from three months of age), and an increase in lactate dehydrogenase release into the medium (p<0.05 from six months of age). By contrast, sex differences were slight. The ‘treatment with 1,2-dichloropropane of slices prepared from rats pretreated with DL-butathionine-[S,R]-sulphoximine significantly increased the depletion of glutathione content (p<0.05) and malondialdehyde release in the medium (p<0.001) caused by the solvent alone.

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