Cortex Of Adult Wistar Rats Research Articles

In-silico analysis of ethanol peel extract of Citrus sinensis on mercury chloride-induced prefrontal cortex damage in Wistar rat

This study evaluated the effect of ethanolic extract of Citrus sinensis peel on mercury chloride-induced changes in the prefrontal cortex of adult Wistar rats. Twenty-five Wistar rats were purchased and divided into five groups containing five animals in each group. Group 1 was administered with distilled water, Group 2, Group 3, Group 4, and Group 5 were administered with 5 mg/kg of mercury chloride only, 5 mg/kg of mercury chloride and 140 mg/kg Silymarin, 5 mg/kg mercury chloride and 1000 mg/kg of ethanoic extract of orange peel, and 5 mg/kg mercury chloride and 1500 mg/kg of ethanoic extract of orange peel. All administration was done orally and the administration lasted for 14 days. The animals were sacrificed humanely using 75 mg/kg ketamine intraperitoneally and prefrontal was dissected out. Part was homogenized in 0.1M phosphate buffered saline for the estimation of superoxide dismutase (SOD), and catalase (CAT) activities, and Malondialdehyde (MDA) level and the other part was fixed by immersion in 10 neutral buffered formal-saline for histological evaluation. The chemical structure of sixteen compounds from Citrus sinensis peel obtained from GC-MS analysis reported in the literature were retrieved from the PubChem compound database and the crystal structure of human peroxisome proliferator- activated receptor gamma (PPARγ; PDB:ID: 2P4Y) reported to increase the expression of catalase gene, human extracellular copper-zinc superoxide dismutase enzyme (PDB ID: 2JLP) and mammalian 15-lipoxygenase - 1 enzyme (PDB ID: 2P0M) responsible for the production of lipid peroxidation were retrieved from the PDB database. Ligands and protein preparation, docking and MM-GBSA relative binding free energy calculation were done in Maestro 2023.1. Data obtained was analyzed using the IBM SPSS (version 25) using one-way ANOVA and p-value < 0.05 was considered statistically significant. The results indicate that the MDA level in control Group(13.29±1.183 μmol) is statistically significantly lower compared to the Group 2 (21.88±1.96 μmol), group 3 (27.44±3.52 μmol), Group 4 (22.20±1.16 μmol) and Group 5 (25.40±3.13 μmol). No statistically significant difference was observed in SOD activity. The CAT activities in control group (53.51±6.83 nmol/ml) was statistically significantly lower compared to the group 2 (26.21±3.70 nmol/ml), Group 3 (27.17±5.32 nmol/ml), Group 4 (25.30±4.24 nmol/ml) and Group5 (26.59±4.22 nmol/ml).The present study suggests, ethanolic extract of Citrus sinensis peel have protective effects on mercury-induced changes in prelimbic part of the prefrontal cortex of adult Wistar rats.

Biochemical and histological analysis of ethanol peel extract of Citrus sinensis on mercury chloride-induced prefrontal cortex damage in Wistar rats

Mercury is one of the heavy metals which is found extensively in many environmental and certain occupational settings. It is the third most dangerous heavy metal and its toxicity causes serious risks to health through unfavorable pathological and biochemical effects. Sweet orange is the fruit of the citrus species (Citrus sinensis) in the family Rutaceae.. Over time there has been increasing interest in the utilization of these peels for both nutritional and medicinal purposes. Studies have reported the antioxidant potential of orange peel oil in laboratory rodents, indicating its protective effect against oxidative stress-mediated ailments. The study evaluated the effect of ethanolic extract of Citrus sinensis peel on mercury chloride-induced changes in the prefrontal cortex of adult Wistar rats. Twenty-five Wistar rats were purchased and divided into five groups containing five animals in each group. Group 1 was administered with distilled water, Group 2, Group 3, Group 4, and Group 5 were administered with 5 mg/kg of mercury chloride only, 5 mg/kg of mercury chloride and 140 mg/kg Silymarin, 5 mg/kg mercury chloride and 1000 mg/kg of ethanoic extract of orange peel, and 5 mg/kg mercury chloride and 1500 mg/kg of ethanoic extract of orange peel. All administration was done orally and the administration lasted for 14 days. The animals were sacrificed humanely using 75 mg/kg ketamine intraperitoneally and prefrontal was dissected out. Part was homogenized in 0.1M phosphate buffered saline for the estimation of superoxide dismutase (SOD), and catalase (CAT) activities, and Malondialdehyde (MDA) level and the other part was fixed by immersion in 10 neutral buffered formal-saline for histological evaluation. The results indicate that the MDA level in control Group(13.29±1.183 μmol) is statistically significantly lower compared to the Group 2 (21.88±1.96 μmol), group 3 (27.44±3.52 μmol), Group 4 (22.20±1.16 μmol) and Group 5 (25.40±3.13 μmol). No statistically significant different that was observed in SOD activity. It CAT activities in control group (53.51±6.83 nmol/ml) is statistically significantly lower compared to the group 2 (26.21±3.70 nmol/ml), Group 3 (27.17±5.32 nmol/ml), Group 4 (25.30±4.24 nmol/ml) and Group5 (26.59±4.22 nmol/ml). Protective role of the extract was observed from the histological evaluation. This study suggests that ethanolic extract of Citrus sinensis peel have protective effects on mercury-induced changes in prelimbic part of the prefrontal cortex of adult Wistar rats.

Subacute Use of Aqueous Extract of Water Melon (Citrullus lanatus) Seeds Mitigates against Pyramidal Neuronal Toxicity of Lead Acetate in Adult Wistar Rats

Introduction: Lead exposure remains a significant public health burden across the globe, impacting millions of individuals and posing a major threat to nervous system development and function As a reported bio-toxic environmental and industrial pollutant, Lead (Pb) do accumulates in almost all body tissues to cause health complications with the cerebellar region of the central nervous system reported to be more susceptible to cellular distortions. As a flowering plant species of the Cucurbitaceae family, watermelon (Citrullus lanatus) is associated with numerous medicinal properties. Aim: This study aim to investigate the possible neuroprotective potential of aqueous extract of citrulus lanatus seed on lead acetates-induced neurotoxicity in the Cerebral cortex of adult Wistar rats. Place of Study: Department of Anatomy, Faculty of Basic Medical Sciences Olabisi Onabanjo University, Ogun State, Nigeria. Methods: Twenty (20) healthy adult female wistar rats weighing 150±50g were randomly assigned into 4 groups (n=5). The Control group received 2mls/kg of distilled water, Treatment group (T1) was administered 7.5 mg/kg of lead acetate, Treatment group (T2) was administered 200 mg/kg of aqueous extract of citrullus lanatus and Treatment group (T3) was administered 7.5 mg/kg of lead acetate and 200 mg/kg of aqueous extract of citrullus lanatus concomitantly orally for fourteen (14) days. H&E and Cresyl violet histological stains and Biochemical assays for SOD, CAT activities and MDA concentration was determined. Data obtained from the study were analyzed using one-way ANOVA and subjected to Turkeys post hoc test from the multiple comparison. Results: Revealed no statistically significant differences (p>0.05) in body weight and brain weight changes across groups relatives to the control group while SOD and Catalase activities were increased significantly in the Treatment groups compared to control group. Histological findings in control group and T2 showed normal histoarchitectural appearance of cerebral cortex Pyramidal neurons while the lead exposed group (T1) revealed features of neurodegenerative changes evident by nuclear shrinkage with pyknosis and karryorrhexis. while T3 revealed near normal presentations. Conclusion: In summary, Citrullus lanatus mitigates against pyramidal neuronal cells distortions following lead acetate induced toxicity in Wistar Rats and also further affirms its antioxidative potential.

Preliminary investigation of the activity of aqueous <i>Cucumis sativus</i> fruit extract on the prefrontal cortex in Wistar rats

Cucumis sativus Linn. is reported to have a wide variety of medicinal uses due to its abundance of carbohydrates, proteins, minerals and secondary metabolites. This study investigated the possible alterations in the prefrontal cortex of adult Wistar rats following the administration of aqueous Cucumis sativus fruit extract (ACSFE). Eighteen (18) Wistar rats, randomly divided into three groups (n=6), were used for this study. Group A served as control while Groups B and C received 250 mg/kg and 500 mg/kg of ACSFE respectively. At the end of the administration, the rats were weighed and the Y-maze test was utilized to evaluate spontaneous alternation of the experimental rats. Thereafter, the cerebri were harvested for antioxidant [Superoxide Dismutase (SOD), Catalase (CAT) and Glutathione (GSH)], lipid peroxidation [Malondialdehyde (MDA)] and histological evaluations. Results showed that there were no significant differences in the final body, absolute whole brain weights and spontaneous alternation of the extract-treated Groups when compared to the control. The histological sections of the prefrontal cortex of the rats in control Group were similar to the extract-treated groups showing normal pyramidal cells with open-face nuclei, basophilic cytoplasm and normal neuroglia cells. Taken together, ACSFE, at these doses, is not toxic to the prefrontal cortex of Wistar rats.

Neurotoxic Effects of Manganese Chloride on the Cerebellar Cortex of Adult Wistar Rats

Manganese is a naturally occurring element and an essential nutrient. It is an essential trace metal that is involved in bone formation, brain development and in the metabolism of carbohydrates, cholesterol and amino acids. Excessive exposure of humans to manganese can result in a neurologic and psychological disorder called Manganism. This study assesses the effect of Manganese on the cerebellar cortex of adult wistar rats. Thirty-six (36) adult wistar rats were picked at random and divided into 4 groups with 9 animals each. Group A which was the control received distilled water, group B, group C and Group D received orally 0.3 mg/kg, 0.6 mg/kg and 0.8 mg/kg body weight of Manganese Chloride respectively for 29 days. Experimental Animals were sacrificed on the 30th day by cervical dislocation. The cerebellum were collected after sacrifice, weighted and fixed in 10% formol calcium and subsequently processed for histological observation using Hematoxylin and Eosin staining principle. Part of the cerebella cortex was homogenized for MDA, NO and SDH analysis. The result shows that the mean body weights decreased significantly in the manganese- treated groups when compared to the control. The mean brain weight of the Manganese Chloride treated groups B, C and D Insignificantly Increased compared with the control. Biochemical analysis of the MDA (Lipid Peroxide), NO (Nitric Oxide) and SDH (Succinate Dehydrogenase) Increased Significantly (P<0.05) in the Manganese treated group compare with the control. Histological analysis showed loss and degenerated neurons particularly the Purkinje cells in the cortical layers of the Manganese treated groups compare with normal Cerebella histoarchitecture in the control. This study concluded that Wistar rats treated with Manganese Chloride demonstrated neurodegenerative changes in the cerebella cortical layers, which may adversely affect some cerebella functions in the Wistar rats investigated.

Neurotoxic effects of manganese chloride on the occipital cortex of adult wistar rats

Manganese (Mn) is the twelveth most abundant element on the earth. It is an essential trace metal that is required for a specific amount of enzymes required for normal cellular functions. Manganese deficiency and intoxication are associated with adverse metabolic and neuropsychiatric effects in humans. This study investigated the effect of manganese chloride on occipital cortex of adult Wistar rats. Thirty-six (36) healthy adult Wistar rats of both sexes weighing between 120 – 200 g were separated into four groups; A, B, C and D. The Wistar rats were subjected to different doses of manganese chloride. The wistar rats in Group A were regarded as the Control which received only feed and distilled water daily for 29 days. Manganese chloride was administered at 10mg/kg, 20mg/kg and 30mg/kg orally to Group B, C and D respectively. The animals were sacrificed on day 30th of the treatment by cervical dislocation. The brain was harvested, weighed with a sensitive weighing balance, Part of the brain was removed and homogenized for biochemical analysis for MDA (Malondialdehyde), NO (Nitric Oxide) and SDH (Succinate dehydrogenase) and the remaining parts were fixed in 10% formol calcium and was processed for histological analysis using H & E staining method. The result showed that the mean body weights of the Wistar rats reduced significantly (P<0.05) in group B , C and D manganese chloride treated group compared with Group A .The brain weights in group B, C and D shows insignificant increase (P>0.05) when compared with group A (control group).The biochemical analysis result showed significant increase (P<0.05) in MDA (Malondialdehyde), NO (Nitric Oxide) and SDH( Succinate dehydrogenase) in the brain of manganese chloride treated groups compared to Control. The histological analysis indicated that occipital cortex shows observable degenerative changes in the occipital cortex characterized by peripheral and central degenerative changes, clustered pyknotic pyramidal and granule neurons that appear with fragmented cytoplasm and condensed nuclei in the manganese chloride treated compared with normal histoarchitecture of occipital cortex in the control. The study concluded that Manganese Chloride treatment has adversely affected the occipital cortical tissue in the treated rats which may affect the occipital cortical functions.

Neurotoxic effects of manganese chloride on the occipital cortex of adult wistar rats

Neurotoxic effects of manganese chloride on the occipital cortex of adult wistar rats

Evaluation of Chronic Administration of Metronidazole on the Morphological and Biochemical Parameters on the Cerebral Cortex of Adult Wistar Rats

Metronidazole has been implicated in diverse neurologic syndromes such as; cerebellar syndrome, encephalopathy, seizures, optic neuropathy, autonomic neuropathy and peripheral neuropathy. Metronidazole is an antibiotic drug used to treat infections of the reproductive system, gastrointestinal tract, skin, heart, bone joint, lung, blood, nervous system and sexually transmitted diseases (STDs). This study therefore, investigated the effects of metronidazole on the cerebral cortex of adult wistar rats.
 Thirty-two (32) adult wistar rats of average weight of 180g of both sexes were distributed into four groups of eight (8) animals per group. Group A was the control group while group B, C and D rats were treated with 250 mg/kg, 500 mg/kg and 1000 mg/kg of metronidazole respectively. Metronidazole was administered orally on daily basis to the animals for 28 days. The weights of the rats were taken weekly using a weighing scale. On the 28th day of the treatment, the animals were sacrificed by cervical dislocation. The skulls were excised and the brains were harvested, weighed immediately using a sensitive weighing balance and then fixed in 10% formolcalcium for routine histological techniques and the other parts were processed for biochemical analysis of Malondialdehyde (MDA), Nitric Oxide (NO) and Succinate dehydrogenase (SDH).
 The results showed that there was a significant increase in the body weights of wistar rats in A and B while the mean body weights of the wistar rats reduced significantly in group C and D. The brain weights in group B and C increased insignificantly while brain weight in group D increased significantly when compared with group A. The biochemical analysis showed significant increase (P<0.05) in the level of MDA, NO and SDH in group B, C and D as compared with group A. Histological study of the cerebral cortex revealed conspicuous degenerative changes in group B while group C and D showed increased degenerative cerebral cortical layers with peripheral and central degenerative changes.
 The study concluded that metronidazole exhibited a neurodegenerative effect on the cerebral cortex of the wistar rats investigated. It is recommended that other studies should be carried out to corroborate these findings.

Neonatal Maternal Separation Modifies Proteostasis Marker Expression in the Adult Hippocampus

Exposure to early-life stress (ELS) can persistently modify neuronal circuits and functions, and contribute to the expression of misfolded and aggregated proteins that are hallmarks of several neurodegenerative diseases. The healthy brain is able to clear dysfunctional proteins through the ubiquitin-proteasome system (UPS) and the autophagy-lysosomal pathway (ALP). Accumulating evidence indicates that impairment of these pathways contributes to enhanced protein aggregation and neurodegeneration. While stress is a known precipitant of neurological decline, few specific mechanistic links underlying this relationship have been identified. We hypothesized that neonatal maternal separation (MatSep), a well-established model of ELS, has the ability to alter the levels of UPS and ALP components in the brain, and thus has the potential to disrupt proteostasis. The expression of proteostasis-associated protein markers was evaluated by immunoblotting in the hippocampus and cortex of adult Wistar rats that were previously subjected to MatSep. We observed multiple sex- and MatSep-specific changes in the expression of proteins in the ALP, mitophagy, and UPS pathways, particularly in the hippocampus of adult animals. In contrast, MatSep had limited influence on proteostasis marker expression in the cortex of adult animals. Our results indicate that MatSep can selectively modify the intracellular protein degradation machinery in ways that may impact the development and progression of neurodegenerative disease.

Neurohistological changes in the cerebellar cortex of adult Wistar rats following lead acetate induced cortical damage

This study investigated the neurohistological effect of lead acetate on cerebellar cortex of adult wistar rats. Lead is a common industrial poisonous substance that its prevalence in the environment exhibits toxic effect which makes different organs & tissues especially the central nervous system vulnerable to lead exposure. Lead is however, found useful applications in diverse items of daily needs like paints, water pipes, car batteries, leaded gasoline, ammunition, cosmetics, hair dye, airplanes, shielding for x-ray machines. Thirty-six (36) adult wistar rats of both sexes weighing between 120-250 grams were randomly grouped into four groups. Group A, B, C and D each group containing seven (9) rats. Group A rats served as the control, and was maintained on standard feed and water for 28 days, group B, C and D rats were treated orally once daily with 0.09g/kg, 0.18g/kg and 0.2g/kg of lead acetate respectively for 28 days. The weights of the wistar rats were recorded on weekly basis during the treatment. All the wistar rats in group A, B, C and D were sacrificed by cervical dislocation on the 29th day of the treatment. The brain was removed and weighed with a sensitive balance and the cerebellum of each rats was then fixed in 10% formol saline, the tissue was processed and stained with Hematoxylin and Eosin for histological study. Results showed that the mean body weights of the wistar rats significantly decreased in the treated groups when compared with the control group. The mean brain weights of the lead treated groups showed a significant decrease when compared to the control group. Histological study of the brain (cerebellar cortex) of the treated groups demonstrated degenerative changes revealed shrinkage, reduced sized and cellular loss of the Purkinje cells with vacuolations in the Purkinje cell layer compared with normal cerebellar histoarchitecture in the control. The study concluded that lead acetate has a neurotoxic effect on the cerebellar cortex of adult wistar rats which may ultimately impair some cerebellar functions.

Neurohistological changes in the cerebellar cortex of adult Wistar rats following lead acetate induced cortical damage

Neurohistological changes in the cerebellar cortex of adult Wistar rats following lead acetate induced cortical damage

Neurodegenerative Observations on the Cerebral Cortex of Adult Wistar Rats Following Mercury Chloride Induced Cortical Damage in Adult Wistar Rats

Background: Mercury is a widespread environmental and industrial pollutant that is used in food preservation, cosmetics, pharmaceutical companies and laboratories. The aim of this present study was to investigate the possible effects of mercury chloride (HgCl2) exposure on the cerebral cortex of adult wista rats; and also to evaluate the effects of mercury on biochemical parameters.
 Materials and Methods: Thirty six (36) adult wistar rats of both sexes, weighing between 110 g-300 g were randomly divided into four groups A, B, C and D with nine animals per group. The animals in groups B, C, and D were administered mercury chloride orally at the concentration of 0.2 mg/kg, 0.4mg and 0.5 mg/kg body weights respectively while group (A) served as control and was given distilled water. The administration lasted for a period of 21 days. The brain was carefully removed and weigh immediately with sensitive balance, part of it was homogenized for biochemical analysis (MDA, GSH and NO). The remaining part was then fixed in 10% formol calcium fluid and processed for histopathological studies using H and E stains.
 Results: The results revealed a decrease in animal body weights from all the groups in comparison with the control group (A) which showed an insignificant decrease (P>0.05), group B showed an insignificant decrease (P>0.05) while group C and D showed statistically significant decrease (P<0.05). The brain weights revealed statistically insignificant decrease in the treated groups when compared with the control group. The biochemical evaluation revealed a statistically significant increase (P<0.05) in the level of MDA (Malondialdehyde) in the treated groups when compared with the control group, GSH (Glutathione) revealed statistically significant decrease (P<0.05) in the treated groups and NO (Nitric Oxide) revealed statistically significant increase (P<0.05) in the treated groups as compared to the control group. The histological observation revealed degenerative changes in the cortex of treated groups that were characterized by clustered Pyknotics pyramidal neurons that appear with fragmented cytoplasm and condensed nuclei within soma. Perineural spaces were seen surrounding degenerating neurons. Axons and dendrites are scarcely appreciable around neurons in these groups.
 Conclusion: The findings from this study showed that ingestion of mercury chloride has potentially deleterious effects on brain as shown in the histopathology, cellular loss in the brain of wistar rat.

Adansonia digitata L. leaf extract attenuates lead-induced cortical histoarchitectural changes and oxidative stress in the prefrontal cortex of adult male Wistar rats

Abstract Objectives Adansonia digitata L. is popularly known for the management of various neurological diseases in ethno-medicine. Studies have shown that lead toxicity is a possible risk factor for early onset of neurodegenerative disease. Hence, this study was designed to evaluate the effect of A. digitata aqueous leaf extract (ADALE) against lead-induced oxidative stress and histo-architectural changes in the prefrontal cortex of adult Wistar rats. Methods Saline (10 mL/kg), ADALE (500 and 1000 mg/kg) and EDTA (55 mg/kg) were pretreated orally 30 min prior to lead acetate (LA) (120 mg/kg) administration to male Wistar rats (n=7) for 21 days. Thereafter, standard biochemical (superoxide dismutate, catalase, glutathionxe and malondialdehyde), histological (H&E) and histochemical assessment (crystyl fast violet stain for nissil substance) were carried out in the prefrontal cortex. Results ADALE significantly (p<0.05) reversed LA-induced oxidative stress, as evidenced by increased catalase, superoxide dismutase and oxidized glutathione levels, and decreased malondialdehyde concentration in the prefrontal cortex. Also, the increase chromatolysis and neuronal pyknosis of the pyramidal neurons of the prefrontal cortex were significantly attenuated by ADALE. Conclusions The result of this study showed that A. digitata aqueous leaf extract attenuated lead acetate-induced cortical neurodegeneration via inhibition of oxidative stress.

Adansonia digitata L. leaf extract attenuates lead-induced cortical histoarchitectural changes and oxidative stress in the prefrontal cortex of adult male Wistar rats.

Objectives Adansonia digitata L. is popularly known for the management of various neurological diseases in ethno-medicine. Studies have shown that lead toxicity is a possible risk factor for early onset of neurodegenerative disease. Hence, this study was designed to evaluate the effect of A.digitata aqueous leaf extract (ADALE) against lead-induced oxidative stress and histo-architectural changes in the prefrontal cortex of adult Wistar rats. Methods Saline (10mL/kg), ADALE (500 and 1000mg/kg) and EDTA (55mg/kg) were pretreated orally 30min prior to lead acetate (LA) (120mg/kg) administration to male Wistar rats (n=7) for 21days. Thereafter, standard biochemical (superoxide dismutate, catalase, glutathionxe and malondialdehyde), histological (H&E) and histochemical assessment (crystyl fast violet stain for nissil substance) were carried out in the prefrontal cortex. Results ADALE significantly (p<0.05) reversed LA-induced oxidative stress, as evidenced by increased catalase, superoxide dismutase and oxidized glutathione levels, and decreased malondialdehyde concentration in the prefrontal cortex. Also, the increase chromatolysis and neuronal pyknosis of the pyramidal neurons of the prefrontal cortex were significantly attenuated by ADALE. Conclusions The result of this study showed that A.digitata aqueous leaf extract attenuated lead acetate-induced cortical neurodegeneration via inhibition of oxidative stress.

English

The present study was aimed at investigating the effect of Cannabis sativa L. administration on neurobehavior and histology of the frontal cortex ofadult Wistar rats. Eighteen (18) adult Wistar rats (120 to 140 g) were divided into three (3) groups of six (6) animals per. Animals in group 1 (control) were given 1 ml/kg distilled water, while groups 2 and 3 were administered with 250 and 500 mg/kg of n-Butanol extract of Cannabis sativa L. respectively via the oral route, daily for 21 days. Motor function was assessed using Ladder rung walking while Haematoxylin and Eosin (H&amp;E) and Cresyl Fast Violet (CFV) stains were used for histological studies of the cerebral cortex. A treatment of rats with 250 and 500 mg/kg showed decrease in foot fault scoring in group 2, and 3 when compared with the control. Also, cytoplasmic vacuolation, dissolution of&nbsp; nucleolus were&nbsp; observed&nbsp; in&nbsp; 250 and 500 mg/kg treatment groups when stained with Haematoxylin&nbsp; and&nbsp; Eosin&nbsp; (H&amp;E) and&nbsp; chromatolysis&nbsp; was&nbsp; observed&nbsp; in&nbsp; 250 mg/kg and 500 mg/kg&nbsp; treatment group. It was concluded that Cannabis sativa L. administration results in motor impairment which could be due to degenerative changes in the cerebral cortex of adults Wistar rats.&nbsp; &nbsp;Key words: Cannabis sativa L., n-butanol, cerebral cortex, Wistar rats, ladder rung walking. &nbsp

The study of the behaviour, the hippocampus and cerebellar cortex of adult Wistar rats exposed to lead and treatment with Psidium guajava leaf extract

The study of the behaviour, the hippocampus and cerebellar cortex of adult Wistar rats exposed to lead and treatment with Psidium guajava leaf extract

Cerebral Cortical Damage in Adult Wistar Rats Following Aluminium Chloride Administration

This study investigated some effects of aluminium chloride on the cerebral cortex of adult Wistar rats. Aluminium chloride as one of the toxic metals has been known to be one of the major environmental pollutants across the world which has been reported in relation to Neurodegenerative diseases (ND) associated with metallic intoxication. It is present in many pharmaceutical drugs, food products and also used in the treatment of domestic water being involved in skeletal, haematological and neurological diseases.&#x0D; Thirty-two adult Wistar of both sexes weighing between 143 g-189 g were randomly grouped into four groups, group A, B, C and D each group containing 8 rats. Group A rats which were the controls, were maintained on standard feed (grower mash) and water for 21 days. Rats in group B, C and D were treated with 0.2 g/kg, 0.4 g/kg and 0.6 g/kg of aluminium chloride respectively for 21days. The aluminium chloride solution was administered orally on a daily basis for that period.&#x0D; The weight of the Wistar rats was recorded on a weekly basis (before and at the end of each week of administration). On the 22nd day the Wistar rats in group A, B, C and D were sacrificed by cervical dislocation, blood was collected through cardiac puncture, the brain was removed and weighed immediately using sensitive balance, part of the brain of all Wistar rats in each group was collected and homogenized for biochemical analysis, the remaining part was then fixed in 10% formol saline, the tissue was processed and sectioned at 5µm and stained with hematoxylin and eosin for histological study.&#x0D; Results showed that the mean body weights of the Wistar rats significantly increased in the treated groups when compared with the control group. The mean brain weights of the aluminium- treated groups showed insignificant decreased (P&gt;0.05) when compared to the control group. In the biochemical analysis, there was a statistically significant increase (P&lt;0.05) in the level of Malondialdehyde (MDA) in the aluminium-treated groups, and a significant decrease (P&lt;0.05) in the level of Superoxide dismutase (SOD), and Succinate Dehydrogenase (SDH) in the aluminium treated group. Histological study of the brain (cerebral cortex) revealed that the cerebral cortical layers of the aluminium treated groups appeared distorted and degenerated, in a dose-dependent manner. The study concluded that aluminium chloride has a neurotoxic effect on the cerebral cortex of adult Wistar rats which invariably may alter some cerebral functions.

Dose-dependent effect of black mustard seeds (Brassica nigra) extract on the prefrontal cortex of adult Wistar rats

Objectives: Mustard seeds, apart from being a culinary essential, have had medicinal applications dating back to the time of Hippocrates. It has in fact been once mentioned as the greatest herb ever. We explored the dose dependent effects of the crude aqueous extract of Brassica nigra (Black mustard seeds) on the prefrontal cortex of adult Wistar rats. Methods: 20 adult female rats weighing an average of 180±20 g were used. They were split into 4 groups (n=5); Group A (received extract at 200 mg/kg body weight), Group B (received extract at 100 mg/kg body weight), Group C (received extract at 50 mg/kg body weight), and Group D (received distilled water ad libitum). All of the animals were subjected to the Y-maze spontaneous alternation test for neurobehavioural analyses following 28-day administration of the extracts. Animals were sacrificed 24 hours after taking the last day of administration. Results: Our results showed that neurobehavioural analyses are significantly hampered in animals receiving 200 mg/kg extract in comparison to the control group. In treatment groups, increased dose of extract elevated the level of MDA, but reduced the level of SOD. LDH levels were also significantly increased in the 200 mg/kg treated group when comparing with the control. General microarchitecture in the prefrontal cortex of 200 mg/kg Brassica nigra treated group showed signs of karyolysis and pyknosis. Conclusion: Brassica nigra (black mustard) is not innocuous and therefore it should be consumed in moderation.

Dietary restriction suppresses apoptotic cell death, promotes Bcl-2 and Bcl-xl mRNA expression and increases the Bcl-2/Bax protein ratio in the rat cortex after cortical injury

Traumatic brain injury (TBI) is one of the leading causes of death and disability in humans.Subsequent pathological events occurring in the brain after TBI, referred to as secondary injury, continue to damage surrounding tissue resulting in substantial neuronal loss. Using an animal model of TBI we examined the effect of dietary restriction (DR) on the neuroapoptosis and Bcl-2 family genes as the main regulators of the intrinsic apoptotic pathway. Bcl-2, Bcl-xl and Bax mRNA and protein expression in the ipsilateral cortex of adult Wistar rats exposed to DR before TBI were studied from 2 to 28 days post injury. Our results showed that DR suppressed neuroapoptosis and promoted significant upregulation of antiapoptotic Bcl-2 and Bcl-xl mRNAs in the ipsilateral cortex following injury. Expression of the proapoptotic Bax gene increased in ad libitum (AL) fed rats but remained unchanged in rats exposed to DR. Although the expression of Bcl-2, Bcl-xl and Bax proteins was changed in a similar manner in both experimental groups, DR promoted a continuous increase in the Bcl-2:Bax protein ratio throughout the recovery period. Together with our previous finding that DR mediates inhibition of the extrinsic apoptotic pathway the present work reveals that modulation of the intrinsic pathway contributes to the beneficial effect of DR in brain injury. These findings provide new insight into the effects of DR on pro-survival signaling after injury, lending further support to its neuroprotective effect.

Lime Juice Induces Ovarian Follicle Degeneration and Reduces Serum Gonadotrophin Level in Rats Model

Background: Lime juice possesses antimicrobial and anti-proliferative property and caused reduced sperm motility in animals. This study aimed at investigating the anti-proliferative effect of lime juice on the ovarian cortex of adult Wistar rats. Methods: Twenty (20) adult Female Wistar rats weighing between 160 190 g were divided into 4 groups (n= 5). Group 1, 2 and 3 received 1 ml/kg, 1.5 ml/kg and 2.23 ml/kg body weight of undiluted lime juice respectively; Group 4 received 0.5 ml of distilled water for period of ten (10) Original Research Article Dare et al.; ISRR, 3(2): 45-51, 2015; Article no.ISRR.2015.008 46 days. Administration was done by gavages oro-gastrically daily using metal oral canula. Animals were sacrificed by cervical dislocation 24 hours after the last administration of lime juice; ovary was dissected out following abdominal incision, fixed in 10% formo-saline for histological observation using H/E stains and blood sample was collected for hormonal (reproductive hormones) assay. Results: Plasma concentration of FSH and LH significantly (p < 0.05) lowered in the lime –treated rats compared with control rats, histological observation revealed degeneration in the follicular cells, stroma hyperplasia and immature follicles in the animals treated with the undiluted lime juice compared with the control group; that revealed follicular cells at different stages of development. Conclusion: Low plasma concentration of FSH and LH observed with consequent degeneration of follicular cells expressed in the ovarian cortex demonstrate anti fertility potential of lime juice.