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Cuprizone is a neurotoxin with copper-chelating ability used in animal model of multiple sclerosis in which oxidative stress has been documented as one of the cascade in the pathogenesis. Moringa oleifera is a phytomedicinal plant with antioxidant and neuroprotective properties. This study aimed at evaluating the ameliorative capability of M. oleifera in cuprizone-induced behavioral and histopathological alterations in the prefrontal cortex and hippocampus of Wistar rats. Four groups of rats were treated with normal saline, cuprizone, M. oleifera and a combination of M. oleifera and cuprizone, for five weeks. The rats were subjected to Morris water maze and Y-maze to assess long and short-term memory respectively. The animals were sacrificed, and brain tissues were removed for histochemical and enzyme lysate immunosorbent assay for catalase, superoxide dismutase, and nitric oxide. Cuprizone significantly induced oxidative and nitrosative stress coupled with memory decline and cortico-hippocampal neuronal deficits; however, administration of M. oleifera significantly reversed the neuropathological deficits induced by cuprizone.

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Permethrin is a common constituent in some household insecticides. This study examined the effects of this chemical on the testicular histology of exposed rats. Fifteen adult male Wistar rats were subgrouped into a control and two treatment groups. The controls were fed on normal rat feeds, whilst the diet of animals in the two treatment groups was mixed with 500 mg/kg and 1000 mg/kg Permethrin respectively. An increase in body weights and organ weights was observed in the animals in both treatment groups. Various degrees of histological alterations in the structure of their seminiferous tubules were also observed in comparison with the control group. These abnormalities included disruption of the normal architecture, reduction in the population of mature sperm cells, wider luminal diameter and reduced interstitial spaces. These effects could impair the fertility potential of male subjects.

Cuprizone-induced neurotoxicity has been employed to study the biology of remyelination in experimental models of multiple sclerosis. This study was aimed at determining the role of kolaviron, a biflavonoid from Garcinia kola, in mitigating the damaging effects of cuprizone on behaviour and the hippocampus. Twenty-four male albino mice aged 6-8 weeks were categorised into 4 equal groups: Group A (Control) received regular diet; Group B received 200 mg/kg/d of kolaviron in addition to their regular diet; Group C received 0.2% cuprizone diet only, while Group D received both kolaviron and cuprizone diet. The treatment lasted for 35 days after which behavioural tests (Morris water maze, Y maze and open field tests) were conducted and brain tissues were processed for histology, histochemistry (Nissl staining), immunohistochemistry (glial fibrillary acidic protein) and biochemistry (malondialdehyde, superoxide dismutase and glutathione peroxidase). Results showed that cuprizone toxicity led to weight loss, impairment in memory and exploratory drive, oxidative stress, chromatolysis and reactive astrocytosis; meanwhile administration of kolaviron prevented cuprizone-induced weight loss, memory decline, oxidative stress and neuromorphological alterations. In conclusion, administration of kolaviron might be useful in limiting the effects of cuprizone toxicity on the morphology and functions of the hippocampus.

To cite this article: Omotoso GO, Olajide OJ, Gbadamosi IT, Rasheed MA, Izuogu CT. Kolaviron protects the prefrontal cortex and hippocampus against histomorphological and neurobehavioural changes in cuprizone model of multiple sclerosis. Malays J Med Sci. 2018;25(2) Abstract Background: This study explored the efficacy of kolaviron-a biflavonoid complex isolated from the seeds of Garcinia kola-in protecting against cuprizone (CPZ)-induced demyelination in both the prefrontal cortex and the hippocampus of Wistar rats.Methodology: Thirty rats were treated to receive 0.5 mL phosphate-buffered saline (group A, control), 0.5 mL corn oil (group B), 0.2% CPZ (group C), for 6 weeks, 0.2% CPZ for 3 weeks and then 200 mg/kg of Kv for 3 weeks (group D), or 200 mg/kg of Kv for 3 weeks followed by 0.2% CPZ for 3 weeks (group E). Rats were assessed for exploratory functions and anxiety-like behaviour before being euthanised and perfused transcardially with 4% paraformaldehyde. Prefrontal and hippocampal thin sections were stained in hematoxylin and eosin and cresyl fast violet stains.Results: CPZ-induced demyelination resulted in behavioural impairment as seen by reduced exploratory activities, rearing behaviour, stretch attend posture, center square entry, and anxiogenic characteristics. Degenerative changes including pyknosis, karyorrhexis, neuronal hypertrophy, and reduced Nissl integrity were also seen. Animals treated with Kv showed significant improvement in behavioural outcomes and a comparatively normal cytoarchitectural profile.Conclusion: Kv provides protective roles against CPZ-induced neurotoxicity through prevention of ribosomal protein degradation.

Abstract:Objectives: This study investigated the adverse effects of excessive consumption of garlic on the small intestine (jejunum and ileum) of adult male Wistar rats.Methodology: Sixteen (16) Wistar rats with average weight of 181.5 g were grouped into two: Control Group A which received distilled water, and Treatment Group B which received 1000 mg/kg/ml aqueous extract of garlic, orally for 28 weeks. The aqueous extraction of raw garlic was done to obtain a concentration of 1000 mg/kg/ml. The animals were sacrificed by cervical dislocation after the last day of administration, and tissues for histological studies were fixed in buffered formalin, while those for enzyme studies were homogenised, and appropriate biochemical kits used to study the activities of acid phosphatase (ACP), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH). Results:The histological sections of the jejunum of animals that received the high dose of aqueous garlic extract revealed the presence of vacuolations, cell death and loss of epithelium, and intact muscle layer; the Periodic-Acid Schiff (PAS) positivity also reduced, while the ileum also showed degeneration of the brush borders, loss of epithelial cells, reduction in the number of goblet cells, vacuolations, and a reduced intensity of PAS positivity. Activities of ACP, ALP and LDH in the jejunum and ileum were increased. Conclusion:Consumption of excessive amount of garlic could cause structural changes to the intestinal tract, which are capable of affecting intestinal functions, such as decrease in glycogen activity in the small intestine, and impairment of the absorptive activities.

This study investigated the neurotoxic effects of permethrin on the cerebellum, hippocampus and prefrontal cortex of Wistar rats and its effects on some behavioral patterns. Fifteen adult male Wistar rats were grouped into three categories: Group A received 0.1 mL normal saline (control), and Groups B and C received mixed feed with 500 mg/kg and 1,000 mg/kg of 0.6% permethrin, respectively, for 14 days. The animals were assessed for memory, anxiety and exploratory locomotion and thereafter anesthetized and transcardially perfused with normal saline and 4% paraformaldehyde (PFA). Cerebellum, hippocampus and prefrontal cortex were excised from the whole brain and processed for tissue histology, histochemistry and immunohistochemistry. Oxidative status and lipid peroxidation were also assessed using catalase, glutathione peroxidase, superoxide dismutase and malondialdehyde as biomarkers. Results revealed dosedependent decrease in body weights but increase in cerebellar and prefrontal weights, depletion of endogenous antioxidant markers, cognitive deficits, reduced locomotor activities, degenerative changes in the microarchitecture at high doses and presence of chromatolytic cells at both low and high doses of permethrin. Astrocytes were activated while synaptophysin expression was downregulated. Permethrin causes dose-dependent neurotoxicity on the morphology, neurochemistry and oxidative status of different brain regions, and these could affect behavioral performance and other neurologic functions.