ANATOMY

Exposure to neurotoxic substances like nickel chloride poses significant risks to neurological health. Vinpocetine, a synthetic derivative of the alkaloid vincamine acts as a phosphodiesterase- 1 inhibitor, modulating intracellular signaling and enhancing cerebral metabolism. It improves cerebral blood flow and supports synaptic plasticity, by increasing cyclic GMP and reducing neuroinflammation and neurodegenerative damage by reducing oxidative stress. Accordingly, this study was aimed at investigating the possible neuroprotective activity of vinpocetine on Nickel Chloride-induced neurotoxicity in adult Wistar rats. In this study, Fourty-two (42) Wistar rats was randomly divided into six (6) groups (n=7). Group A rats served as the control group to be given 1ml of distilled water. Group B rats was administered Nickel Chloride only at a dose of 5mg/kg body weight. Group C rats was administered 2.5mg/kg body weight of Vinpocetine and 5mg/kg body weight of Nickel Chloride. Group D rats was administered 5mg/Kg body weight of Vinpocetine and 5mg/kg body weight of Nickel Chloride. Group E rats was administered with 2.5mg/Kg body weight of Vinpocetine only and group F rats was administered with 5mg/Kg body weight of vinpocetine. Neurobehavioral activities were assessed 24 hours before the last administration, and at the end of the experimental period, the rats were weighed and sacrificed, and the body and brain weight changes, antioxidant enzymes activity, as well as histological assessment of the cerebrum. Results indicate that nickel chloride administration led to significant decrease on body weight, brain weight, neurobehavioral activity, and antioxidant enzymes levels, while increasing lipid peroxidation. However, pretreated rats with Vinpocetine mitigated these detrimental effects induced by nickel chloride. Vinpocetine supplementation was associated with improved body and brain weight, enhanced neurobehavioral performance, elevated antioxidant enzyme levels. This study sheds light on vinpocetine's potential as a neuroprotective agent against nickel chloride-induced neurotoxicity, suggesting its importance in preventing or mitigating neurological disorder caused by nickel chloride.

Cerebellar disorders are a class of neurological impairments characterized by unsteady gait anduncoordinated movements, typically resulting from lesions or pathologies affecting the cerebellum. These disorders may arise from congenital anomalies, hereditary ataxias, or exposure to environmental neurotoxicants such as heavy metals. Mercury, a highly toxic heavy metal, is known to exert deleterious effects on the central nervous system. Its lipophilic nature enables it to cross the blood-brain barrier, where it accumulates and induces oxidative stress, leading to neuroinflammation, neuronal damage, and impaired motor coordination. Dietary antioxidants have shown promise in combating mercury-induced neurotoxicity. Accordingly, this study investigated the activity of ethanol extract of Pleurotus ostreatus (P. ostreatus) against mercuric chloride (HgCl2) induced cerebellar toxicity in Wistar rats. In this study, fortytwo (42) Wistar rats were randomly assigned into six groups (A-F). Group A rats served as control; Group B received 4 mg/kg body weight [bw] of HgCl2 only; Group C received 4 mg/kg bw of HgCl2+ 250 mg/kg of P. ostreatus; Group D received 4 mg/kg bw of HgCl2 + 500 mg/kg of P. ostreatus; Group E received 250 mg/kg bw of P. ostreatus only and Group F received 500mg/kg bw of P. ostreatus only. All administrations were done orally for twenty-eight (28) days. Neurobehavioural activity was subsequently evaluated using the Open Field, String, Movement Initiation and Step Tests. Following the assessments, the experimental rats were sacrificed via cervical dislocation and the cerebellum harvested for antioxidant enzymes activity, lipid peroxidation, mercury concentration and histological assessments. The findings revealed that rats exposed to HgCl2 exhibited significant (p <0.05) weight loss, motor deficit, impaired antioxidant defense, elevated lipid peroxidation, elevated mercury levels and degeneration of Purkinje cells and molecular layer neurons. However, co-administration with P. ostreatus significantly (p < 0.05) mitigated these mercury-induced cerebellar alterations in Wistar rats. Overall, the findings from this study indicate that P. Ostreatus mitigates mercuric chloride-induced cerebellar toxicity, primarily through its antioxidant, neuroprotective, and metal-chelating properties, thus making it a promising agent for the development of novel therapeutic strategies aimed at managing mercury neurotoxicity and its associated motor impairments.

Hippocampal dysfunction is a key feature of several neurocognitive disorders and may arise from factors such as congenital defects, neurodegeneration, or exposure to neurotoxicants. Lead (Pb), a potent heavy metal, crosses the blood-brain barrier and accumulates in the hippocampus, where it disrupts calcium signaling and induces oxidative stress, thus contributing to neuronal damage and cognitive deficits. Evidence suggests that dietary antioxidants may help mitigate Pb-induced oxidative damage and preserve hippocampal function. Accordingly, this study investigated the protective activity of aqueous Rosmarinus officinalis leaf extract (R. officinalis) against lead acetate (PbA) induced hippocampal toxicity. Forty-eight (48) adult Wistar rats were randomly assigned into six groups (A-F). Group A served as control; Group B received 100 mg/kg body weight [bw] of PbA only; Group C received 100 mg/kg bw of R. officinalis extract and PbA; Group D received 200 mg/kg bw of R. officinalis extract and PbA; Group E received 100 mg/kg bw of R. officinalis extract only and Group F received 200 mg/kg bw of R. officinalis extract only. All administrations, via an orogastric tube, lasted for twenty-eight (28) days. Thereafter, neurobehavioral activities were evaluated using the Novel object recognition, Y-maze and Elevated plus maze tests. Following the sacrifice of the experimental rats, the hippocampi were collected for Pb concentration, antioxidant enzymes activity, lipid peroxidation, acetylcholinesterase activity, nitric oxide levels, and histological assessments as well as apoptosis. The findings showed that PbAexposed rats exhibited significant (p<0.05) weight loss, cognitive and memory impairments, dysregulated antioxidant enzymes activity, and increased lipid peroxidation, nitric oxide, Pb and AChE levels, along with atrophy and vacuolation of pyramidal cells and astrocytes in the CA1 region of the hippocampus. Also, there was an upregulation of Caspase-3 expression in the hippocampus of experimental rats exposed to PbA, indicating apoptosis as a possible mechanism of action. However, pretreatment with R. officinalis significantly (p<0.05) mitigated the adverse effects induced by PbA in the hippocampus of experimental rats suggesting strong metal-chelating, anti-cholinesterase, and NO-scavenging effects. Similarly, the downregulation of caspase-3 expression in the hippocampus of PbA-exposed rats following pretreatment with R. officinalis supports its anti-apoptotic potential. Overall, these findings suggest that R. officinalis exhibits potent antioxidant, metal-chelating, nitric oxide-scavenging, anti-cholinesterase and anti-apoptotic properties, thus providing novel evidence supporting R. officinalis as a promising neuroprotective agent with potential for drug development against hippocampal dysfunction.

An Experimental Study in Adult Wistar Rats Metal poisoning and its impact on human health have increased due to industrialization and anthropogenic activities. This study aims to investigate the effect of glycine on cadmium-induced gastric damage in adult Wistar rats. Thirty rats were divided into six groups, including control, cadmium only, glycine only, and combinations of cadmium and glycine. Various biochemical markers were assessed, including oxidative stress indicators (SOD, MDA, CAT) and total protein. Histological analyses were performed on stomach tissues. Cadmium administration led to reduced body weight and
increased malondialdehyde (MDA) levels, indicating oxidative damage. Superoxide dismutase (SOD) activity decreased, revealing compromised antioxidant defenses. However, catalase activity was largely unaffected by cadmium. Interestingly, glycine administration showed positive effects. It attenuated cadmium-induced MDA increase, maintained glutathione levels, and improved SOD activity. It also increased total protein levels. Histological observations demonstrated that cadmium induced inflammatory responses, muscle degeneration, and congestion in the stomach. Glycine treatment mitigated these effects, leading to near-normal
tissue architecture. This study demonstrates that cadmium exposure can lead to oxidative stress and cellular damage, while glycine supplementation can exert a gastro-ameliorative effect by enhancing antioxidant defenses, maintaining glutathione levels, and mitigating histological alterations. These findings offer insight into the potential therapeutic benefits of glycine against cadmium-induced gastric damage. Glycine's availability and safety make it a promising avenue for further research and development of affordable gastro-ameliorative interventions

Herbal extracts which can serve as medicinal plants have been used since ancient times and even considered the source of modern medicine. Bry Hullum pinetum extracts have been shown to possess neuroprotective properties potentially useful in treating neurodegenerative diseases. Podophyllum pinetum is a plant used to treat inflammations, infections, and also have anti cancer properties. This study was carried out to explore the effects of Podophyllum pinetum extract on the cerebrum of Adult Wistar rats. A total of thirty (30) rats weighing between 140g-200g were randomly assigned into six (6) groups (A,B,C,D,E and F),with five rats per group. Group A was control group while Group B,C,D,E and F were administered with Podophyllum pinetum extract in doses of 200,400,600,800 and 1000mg/kg respectively. The rats were acclimatized for a period of two weeks and administered for a period of four weeks using oral route by the use of orogastric tube. The rats were
anesthetized with chloroform and then sacrificed. The cerebrum was harvested and immediately fixed for antioxidant stress test and for tissue processing. H&E stains were use for histological test. The result of the study shows that there was no statistically significant difference (P<0.05) in the final body weight of rats in entire group compared to it's initial body weigh except group B where there is a significant change in weight .There was no statistically significant difference (P<0.05) in cerebrum weight and organo-somatic index. In the chart showing the antioxidant results, it shows that it is not statistically significant. Histological slides in control group show: molecular, external granular, external pyramidal, internal granular, internal pyramidal and multi-form layers. Group B show: vasodilatation normal pyramidal neurons with conspicuous nucleoles oligodendrocytes and neuropil. Group C show: normal neurons with conspicuous nucleoles, oligodendrocytes, neuropil cerebral vasodilatation. Group D show: normal granular cell neurons with conspicuous nucleoli, normal oligodendrocytes and marked vasodilatation and active congestion. Group E and F marked show vasodilatation and active congestion, normal granular cells with conspicuous nucleolus and oligodendrocytes. In conclusion, graded concentration of Podophyllum pinetum induced vasogenic effects and increased protein synthesis in a dose dependent fashion and it had no adverse effect on it