ABSTRACT
Prolonged separation of pups from their mother in early postnatal period can interfere with normal growth and development, resulting in different behavioral changes similar to features of schizophrenia in man. This study explored the cytoprotective action of kolaviron, a biflavonoid, on the prefrontal cortex and hippocampus of maternally deprived Wistar rats. Eight months old female rats were time-mated, and after delivery their pups were randomly assigned into four groups; group A received 0.5 ml of normal saline, group B received kolaviron orally (200 mg/kg/bw) on postnatal days (PND) 21–35, group C were maternally deprived on PND 9 for 24 hours, while group D were also maternally deprived on PND 9 for 24 hours, and then received kolaviron orally (200 mg/kg/bw) on PND 21–35. Behavioral studies (open field test, Morris water test, and Y-maze test) were conducted after the experiment prior to sacrifice. Some of the rats were anesthetized with ketamine and perfusion-fixed with 0.1 M phosphate buffered saline and 4% paraformaldehyde, while others were sacrificed by cervical dislocation for enzyme studies. The hippocampus and prefrontal cortex were excised from the brain and processed for tissue histology, histochemistry, and enzymatic analysis. Results revealed behavioral deficits, oxidative stress, degenerative changes, and astrocytosis in the prefrontal cortex and hippocampus of maternally deprived rats, but intervention with kolaviron caused significant improvement in neurobehavior, morphology, and neurochemistry in these brain areas. We concluded that kolaviron could protect the brain against neurological consequences of nutritional and environmental insults arising from maternal separation in early postnatal period.
ABSTRACT
Prolonged separation of pups from their mother in early postnatal period can interfere with normal growth and development, resulting in different behavioral changes similar to features of schizophrenia in man. This study explored the cytoprotective action of kolaviron, a biflavonoid, on the prefrontal cortex and hippocampus of maternally deprived Wistar rats. Eight months old female rats were time-mated, and after delivery their pups were randomly assigned into four groups; group A received 0.5 ml of normal saline, group B received kolaviron orally (200 mg/kg/bw) on postnatal days (PND) 21–35, group C were maternally deprived on PND 9 for 24 hours, while group D were also maternally deprived on PND 9 for 24 hours, and then received kolaviron orally (200 mg/kg/bw) on PND 21–35. Behavioral studies (open field test, Morris water test, and Y-maze test) were conducted after the experiment prior to sacrifice. Some of the rats were anesthetized with ketamine and perfusion-fixed with 0.1 M phosphate buffered saline and 4% paraformaldehyde, while others were sacrificed by cervical dislocation for enzyme studies. The hippocampus and prefrontal cortex were excised from the brain and processed for tissue histology, histochemistry, and enzymatic analysis. Results revealed behavioral deficits, oxidative stress, degenerative changes, and astrocytosis in the prefrontal cortex and hippocampus of maternally deprived rats, but intervention with kolaviron caused significant improvement in neurobehavior, morphology, and neurochemistry in these brain areas. We concluded that kolaviron could protect the brain against neurological consequences of nutritional and environmental insults arising from maternal separation in early postnatal period.
ABSTRACT
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.
Subject(s)
Animals , Rats , Brain , Catalase , Cuprizone , Hippocampus , Memory , Memory, Short-Term , Models, Animal , Moringa oleifera , Moringa , Multiple Sclerosis , Neurons , Nitric Oxide , Oxidative Stress , Plants , Prefrontal Cortex , Rats, Wistar , Superoxide Dismutase , WaterABSTRACT
Background: This study explored the efficacy of kolaviron—a biflavonoid complex isolatedfrom the seeds of Garcinia kola—in protecting against cuprizone (CPZ)-induced demyelination inboth the prefrontal cortex and the hippocampus of Wistar rats.Methodology: Thirty rats were treated to receive 0.5 mL phosphate-buffered saline (groupA, control), 0.5 mL corn oil (group B), 0.2% CPZ (group C), for 6 weeks, 0.2% CPZ for 3 weeks andthen 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 behaviourbefore being euthanised and perfused transcardially with 4% paraformaldehyde. Prefrontal andhippocampal thin sections were stained in hematoxylin and eosin and cresyl fast violet stains.Results: CPZ-induced demyelination resulted in behavioural impairment as seen byreduced exploratory activities, rearing behaviour, stretch attend posture, center square entry,and anxiogenic characteristics. Degenerative changes including pyknosis, karyorrhexis, neuronalhypertrophy, and reduced Nissl integrity were also seen. Animals treated with Kv showedsignificant improvement in behavioural outcomes and a comparatively normal cytoarchitecturalprofile.Conclusion: Kv provides protective roles against CPZ-induced neurotoxicity throughprevention of ribosomal protein degradation.