DEPARTMENT OF ANATOMY

Cerebellar dysfunction, marked by impaired coordination and balance, often result from toxic or degenerative damage to cerebellar neurons. Excessive exposure to manganese chloride, a neurotoxic compound, disrupts neuronal integrity through oxidative stress and inflammation, leading to motor and structural deficits. Vanillin, a natural phenolic compound with strong antioxidant and anti-inflammatory properties, has shown potential in mitigating such neurotoxic effects. This study therefore investigated the protective effect of vanillin against manganese chloride–induced cerebellar toxicity in Wistar rats. Forty-eight (48) Wistar rats were randomly assigned into six groups (A-F). Group A rats served as the control group; Group B rats were administered 10 mg/kg body weight of manganese chloride; Group C rats were administered 20 mg/kg body weight of vanillin and 10 mg/kg body weight of manganese chloride; Group D was administered 40 mg/kg body weight of manganese chloride and 40 mg/kg body weight of vanillin; Group E was administered 20 mg/kg body weight of vanillin; Group F was given 40 mg/kg body weight of vanillin. All administrations lasted for twentyeight (28) days. Neurobehavioural activities were evaluated using the open field, movement initiation, step and string Tests. Results from the study revealed that rats exposed to manganese chloride exhibited significant (p<0.05) weight loss, motor deficit, impaired antioxidant defense, elevated lipid peroxidation and degeneration of Purkinje cells and molecular layer neurons. However, pre-treatment with Vanillin significantly (p<0.05) mitigated these manganese chloride-induced cerebellar alterations in Wistar rats. Overall, the findings from this study indicate that vanillin possesses strong antioxidant properties, supporting its potential as an effective therapeutic agent for the treatment and management of manganese chlorideinduced cerebellar dysfunction

Musa paradisiaca (plantain) is widely used in traditional medicine and consumed as food, yet its renal safety profile remains poorly characterized. This study evaluated the dose dependent
effects of its aqueous extract on kidney function and oxidative stress in adult Wistar rats. Twenty-five rats were divided into five groups (A–E) and administered control, 100, 500, 750, and 1000 mg/kg of Musa paradisiaca extract orally for 16 days. Serumurea, creatinine, antioxidant enzymes—superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase(GPx)—and malondialdehyde (MDA) were assayed. Kidney weights, reno-somatic index(RSI), and histological features were evaluated. Serum urea increased significantly (p < 0.05) inratsreceiving 750 mg/kg and 1000 mg/kg extract compared with control. Antioxidant enzymeactivities (SOD, CAT, and GPx) declined notably at higher doses, whereas MDA levels hadnosignificantly, indicating absence of enhanced lipid peroxidation and oxidative stress. TheRSIwas elevated in the 1000 mg/kg group, although body weights were unaffected. Histological
sections showed preserved renal architecture across groups, suggesting functional rather than structural injury at higher doses. In conclusion the aqueous extract of Musa paradisiacaislargely safe at low to moderate doses but elicits biochemical signs of nephrotoxicity at higher concentrations. The findings justify the need for dosage regulation and caution in prolonged or high dose use of plantain based remedies

Nickel chloride (NiCl2) is a widespread environmental contaminant that causes neurotoxicity, with the cerebellum showing particular vulnerability due to its central role in motor coordination and high metabolic demands. Memantine, a non-competitive
N-methyl-D-aspartate (NMDA) receptor antagonist. It is hypothesized that its neuroprotective properties could be beneficial in the mitigation of cerebellar damage caused by nickel chloride. This study was aimed at investigating the effects of memantine on the nickel chloride induced cerebellar toxicity in wistar rats. Forty-eight rats were divided into eight groups: Control, nickel chloride only, high dose of memantine + nickel chloride, low dose of memantine + nickel chloride, high dose of memantine, low dose of memantine. The treatment protocol ran for 28 days. A served as control and received 1ml of distilled water daily to compensate for stress of administration, whereas, rats in group B received 2.5mg/kg of NiCl₂, rats in group C received 10mg/kg Og memantine(low dose) and 2.5mg/kg of NiCl₂, rats in group D received 20mg/kg of memantine (high dose) and 2.5mg/kg of NiCl₂, rats in group E received 10mg/kg of memantine (low dose) and rats in group F received 20mg/kg of memantine (high dose). Administration of memantine was done orally using an orogastric tube while the administration of nickel chloride was done via intraperitoneal injection. It lasted for 28days. The body weight of the rats were recorded daily. At the end of the experimental period, the rats were sacrificed by cervical dislocation and the organ( cerebrum) weight was recorded. The parameters accessed include cerebral antioxidant enzymes (SOD, CAT, GPx and GSH), MDA concentration and the histology of the cerebrum using
Hematoxylin and Eosin staining technique. Results obtained showed no significant change (p>0.05) in the initial body weight and final body weight. A significant decrease (p<0.05) was observed in the weight change of rats in group B when compared to control, however, a significant increase (p<0.05) was observed in the weight of groups C and D when compared to group B. No significant change (p>0.05) was observed in the cerebellar and relative cerebellar weight of rats across experimental groups. A significant decrease (p<0.05) was observed in cerebellar SOD, CAT, GPx and GSH activity of rats in group B (2.5 mg/kg bw. NiCl2) when compared to the control. A significant increase (p>0.05) in cerebellar MDA concentrations was observed in the weights of rates in group B (2.5 mg/kg bw. NiCl2 ) when compared with group A. Severe histological alterations in the cerebellum of nickel-chloride exposed rats were observed. However, pre-treatment with memantine mitigated the adverse effects induced by NiCl2. In conclusion, findings from this study shows that memantine exerted antioxidant properties as well as mitigating the histological alterations in the cerebellum.

Lawsonia inermis commonly known as henna has been used traditionally, especially in ayurvedic medicine, for various conditions including liver ailments, and reported to have hepatoprotective properties. This study aims to study the effect of aqueous extract of L.
inermis leaves in acute ethanol induced hepatic damage in adult Wistar rats. Thirty (30) female rats were equally divided into five (5) groups (I-V). Group I which served as control received distilled water for 28 days. Group II received Lawsonia inermis for 28 days. Group
III received 100 mg/kg of lead acetate only for 28 days. Group IV simultaneously received 100 mg/kg of lead acetate and treated with 70mg/kg of silymarin for 28 days to serve as reference drug. Group V simultaneously received 100mg/kg of lead acetate and treated with
200mg/kg of L. inermis for 28 days. Group VI simultaneously received 100mg/kg of lead acetate and treated with 400mg/kg of L. inermis for 28 days. Group VII received 400mg/kg of L. inermis and followed with 100mg/kg of lead acetate after 30 minutes for 28 days. All
animals were sacrificed on the twenty ninth (29th) day. Body weight changes and liver body weight index were determined. Liver tissues were collected for assessment of enzymes concentration, and also for haematoxylin and eosin staining. Body weight increased in all
groups from initial mean weight of 180.1 g, though significantly (p<0.05) only in Group IV, Group V and Group VI. Liver body weight index was highest in Group I, and was significantly (p<0.05) different from Group III and Group V. Lead administration reduced level of enzyme aspartate Transferase significantly and increased the value of total bilirubin significantly of (P<0.05) although decrease was seen in enzymes like unconjugated bilirubin, alkaline phosphate and alanine Transferase and increased in conjugated bilirubin but these
were not significant to (P<0.05) H&E staining revealed attenuation of the effects of Lead administration by the extract and silymarin, though the extract proved more effective at 400 mg/kg dose and duration of 28 days. Promising result was also observed in the group that
received 200mg/kg dose over a duration of 28 days.

Many different forms of exposure to Cadmium have been shown over the past century with Cadmium
been present in the environment as a result of many human activities. The constant sources of Cadmium
contamination are related to it's application in industry as a corrosive reagent, as well as it's use as a stabilizer in PVC products, color pigments and Ni-Cd batteries. In areas with contaminated soils, house dust is a potential route for cadmium exposure. Cadmium exposure causes pathological conditions such as neurodegenerative diseases, Alzheimer's disease and Parkinson's disease. Medicinal drugs have been
administered to fight the effect on humans. Due to this, many plants have been discovered for the treatment of the disease caused by Cadmium. Turmeric is one of the medicinal plants which contains anti- oxidant and anti-inflammatory properties which helps to fight against oxidative stress caused by Cadmium. It helps fight against neurodegenerative diseases. Accordingly, this research was designed to
evaluate the protective activity of the ethanolic Curcuma longa root extract on cadmium-induced hippocampal damage in adult Wistar rats. For this study period of twenty-one days, thirty adult Wistar rats were randomized into six groups(A-F) consisting of five rats each. The rats were left to acclimatize for two weeks after which their weights were taken and recorded as initial weights while feeding then
with standard rat chow and free access to water throughout the study. All administration, given orally, started with Group A serving as the control group and received 1ml of water. Group B was given 5mg/kg
body weight of Cadmium only. Groups C and D were given 100mg and 200mg/kg body weight of ethanolic Curcuma longa root extract and 5mg/kg body weight of cadmium respectively. Groups E and F
were given only 100mg and 200mg/kg body weight of ethanolic Curcuma longa root extract, respectively. At the end of the experiment, neurobehavioural activity (y-maze test) was evaluated, recorded, and the rats were then sacrificed for sample collection. Following appropriate harvesting of the hippocampus, the antioxidant activity and histological alterations were investigated. Results showed a significant decrease in the brain and body weight of rats treated with cadmium. For the Y-maze test, Curcuma longa demonstrated significant inhibition of Cadmium-induced cognitive dysfunction. Curcuma longa produced a significant decrease in MDA level and increased SOD, CAT, GPx enzymes as compared to the Cadmium treated group. The histology of rats pre-treated with ethanolic Curcuma longa root extract showed considerable retention of the normal histological morphology of the hippocampus. In conclusion, the findings of the study validated the toxicity of cadmium and provided the first research evidence of the protective activity of Curcuma longa against cadmium toxicity in adult Wistar rats.

Alcohol (ethanol) is a widely consumed psychoactive substance known to induce oxidative stress and gastrointestinal mucosal damage, particularly in the duodenum. Chronic alcohol exposure generates reactive oxygen species (ROS) and disrupts mucosal integrity. Melatonin, a neurohormone synthesized in the pineal gland and gastrointestinal tract, exhibits antioxidant and anti-inflammatory properties, and may offer protection against alcohol-induced tissue injury. To Investigate the Effects of Melatonin on Alcohol induced duodenal Toxicity in Adult Wistar Rats. Twenty adult male Wistar rats were randomly divided into four groups (n=5): control, alcohol only (50% ethanol), melatonin only (5 mg/kg), and melatonin plus alcohol. All treatments were administered orally via gavage for 28 days. After the exposure period, blood samples were collected to assess oxidative stress markers, and duodenal tissues were harvested for histopathological analysis. Statistical analysis were performed using one-way ANOVA with significance set at p<0.05. Alcohol induced ulcer in the mucosa of the duodenum and the ulcer induced was a funnel shaped. The group given melatonin and alcohol showed protective effect, preventing alcohol induced ulceration. In conclusion, melatonin at 5mg/kg prevented against alcohol-induced duodenal ulceration in wistar rats.

Isotretinoin (Accutane), a retinoid commonly prescribed for severe acne, has been shown to induce oxidative stress and organ toxicity during pregnancy, leading to developmental abnormalities in the fetus. The liver and kidneys are particularly prone to Accutane-induced damage due to their vital roles in detoxification and excretion. Previous studies has shown that quercetin scavenges free radicals and inhibits lipid peroxidation, while vitamin E stabilizes cell membranes and enhances antioxidant defense mechanisms. This study investigated the attenuating effects of quercetin, a natural flavonoid with antioxidant and anti-inflammatory properties, and vitamin E, a lipid-soluble antioxidant, on Accutane-induced liver and kidney toxicity during prenatal development. Pregnant Wistar rats were divided into four groups of five animals each: Control, Accutane only, Accutane + Vitamin E, and Accutane + Quercetin + Vitamin E. Administration was carried out from gestation day 14–21, and the littered fetuses
were sacrificed on postnatal day 30 for biochemical and histological analyses. Data was analysed using the SPSS statistical tool. Results showed that exposure to Accutane led to reduced birth weight and crown-rump length compared to other groups, while co-treatment with quercetin and vitamin E improved birth weight comparable to the control. Histological findings of the Accutane-only and Accutane + Vitamin E groups showed periportal inflammation in the liver while the Accutane-only group showed interstitial congestion and tubular swelling in the kidneys, both markedly reduced by co-treatment. In conclusion, the
combination of quercetin and vitamin E significantly attenuated Accutane-induced hepatorenal toxicity, highlighting their potential as protective antioxidants for maternal and fetal health

Hippocampal dysfunction, often linked to learning and memory impairments, can result from neurodegeneration or exposure to toxic agents. Manganese chloride, a neurotoxic compound, accumulates in the hippocampus and disrupts neuronal signalling through oxidative stress, mitochondrial dysfunction, and inflammation, leading to cognitive deficits. Vanillin, a natural phenolic compound with antioxidant and anti-inflammatory properties, has shown potential in protecting against such neurotoxic damage and preserving hippocampal integrity. Accordingly, the aim of this study was to evaluate the activity of vanillin on manganese chloride-induced hippocampal toxicity in Wistar rats. Forty-eight (48) adult Wistar rats were randomly assigned into six groups (A-F). Group A served as control; Group B received 10 mg/kg body weight [BW] of manganese chloride only; Group C received 20 mg/kg BW of vanillin and 10 mg/kg BW of manganese chloride. Group D received 40 mg/kg BW of vanillin and 10 mg/kg BW of manganese chloride. Group E received 20 mg/kg BW of vanillin only and Group F received 40 mg/kg BW of vanillin only. All administrations, lasted for twenty-eight (28) days. Nneurobehavioral activities were evaluated using the Novel object recognition and elevated plus maze tests.

The cerebrum, vital for cognition and motor control, is highly susceptible to toxic injury. Excess manganese chloride exposure induces oxidative stress, mitochon drial dysfunction, and neuroinflammation, resulting in cerebral degeneration. Vanillin, a natural antioxidant and antiinflammatory agent, may counter these effects. Thus, this study aimed to investigate the activity of vanillin against manganese chloride–induced cerebral toxicity in adult Wistar rats. Forty-eight (48) Wistar rats were randomly assigned into six groups (A-F). Group A rats served as the control group; Group B rats were administered 10 mg/kg body weight of manganese chloride; Group C rats were administered 20 mg/kg body weight of vanillin and 10 mg/kg body weight of manganese chloride; Group D was administered 40 mg/kg body weight of manganese chloride and 40 mg/kg body weight of vanillin; Group E was administered 20 mg/kg body weight of vanillin; Group F was administered 40 mg/kg body weight of vanillin. All administrations lasted for twenty-eight (28) days. Neurobehavioural activities were evaluated using the Y-Maze Test. Results from the study showed manganese chloride-exposed rats showed significant (p<0.05) weight loss, cognitive deficits, decreased antioxidant enzymes activity, and increased lipid peroxidation with vacuolization and pyknotic nuclei observed in the cerebrum histology

The use of traditional medical therapy is an important method in the treatment and management of diseases in the African continent and this could be as a result of social, cultural and economic lifestyles. Pharmacologically, the active ingredients found in pyrenacantha staudtii can be extracted and used to cure and prevent numerous diseases. The aim of this research was to investigate the effect of aqueous extract of pyrenacantha staudtii on the undamaged spleen of adult wistar rats. Thirty adult wistar rats weighing between 110g and 200g were used for this experiment with five rats in each group. All rats were allowed two weeks of acclimatization and they all had equal access to feed and water. Group A was the control and was not administered with any extract. Group B was administered with a low dose of the extract(100mg). Group C was administered with a medium dose of the extract(200mg). Group D was administered with 400mg of the extract. Group E was administered with 800mg of the extract. Group F was administered with 1600mg of the extract. All the rats were administered with the extract for 35 days. On the 36th day, the rats were sacrificed via chloroform anaesthesia and the spleen were harvested immediately and preserved in 10% formal saline for tissue processing using H&E for histological analysis