Calcium Supplementation Ameliorates Cerebellar Oxidative Stress in Lactational Aluminum-induced Neurotoxicity in Rats.

Introduction: The neurotoxic effects of aluminum exposure during the critical period of neurodevelopment have been well documented. This study investigated the known protective effects of calcium supplementation on the cerebellum of juvenile Wistar rats following aluminum-induced neurotoxicity during lactation. Methods: Four groups of juvenile rats were exposed via lactation to distilled water (control group), aluminum (40 mg/kg/d), calcium supplement (50 mg/kg/d), and a combination of both aluminum and calcium from postnatal day 4 to day 28. The cerebella of the animals were excised to access the levels of antioxidant enzymes (superoxide dismutase [SOD], glutathione peroxidase [GPx]), lipid peroxidation (malondialdehyde), histomorphological alterations (hematoxylin and eosin staining), Nissl profile (cresyl fast violet staining), and glial activation (glial fibrillary acidic protein immunohistochemistry). Results: Lactational aluminum significantly decreased the activities of superoxide dismutase and glutathione peroxidase while exacerbating lipid peroxidation and reactive astrocyte in cerebellar lysates. Lactational calcium supplementation normalized the activities of SOD and GPx, thereby preventing excessive lipid peroxidation and glial activation. Despite no apparent changes in the general histology of the cerebellum, aluminum-induced chromatolysis changes in the Purkinje cell layer, which was counteracted by the antioxidant propensities of calcium supplementation. Conclusion: These findings support that calcium supplementation significantly protects the cerebellum against aluminum-induced oxidative stress, chromatolysis, and neuroinflammation.

Ameliorative effects of Moringa on cuprizone-induced memory decline in rat model of multiple sclerosis.

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.

Kolaviron protects the brain in cuprizone-induced model of experimental multiple sclerosis via enhancement of intrinsic antioxidant mechanisms: Possible therapeutic applications?

Multiple sclerosis is a demyelinating condition of the central nervous system which commonly affects young adults. Kolaviron, a biflavonoid isolate of Garcinia kola, has been used in experimental studies which explored its anti-oxidative, anti-inflammatory and anti-genotoxic properties. This work was aimed at unraveling the possible ameliorative effect of kolaviron on cuprizone-induced demyelination in the prefrontal cortices of Wistar rats. A total of 28 adult male Wistar rats were divided into four groups A-D. Group A received corn oil (Control), group B received 0.2% Cuprizone, group C received kolaviron (200 mg/kg bw), while group D rats were treated concomitantly with both kolaviron and cuprizone. All groups were treated for 42 days, after which behavioral, histological, immunohistochemical and biochemical analyses were carried out on the prefrontal cortices. Cuprizone significantly down-regulated the level of superoxide dismutase, exacerbated lipid peroxidation and, reduced spatial memory. Cuprizone also induced peripheral and central chromatolysis alongside with atrophied astrocytes in the prefrontal cortex. These alterations were significantly prevented in kolaviron-treated rats, as kolaviron sustained the integrity of neuronal and non-neuronal cells. The activity of kolaviron observed in this study was due to its intrinsic antioxidant properties, which enabled it to combat oxidative damage induced by cuprizone, thereby making kolaviron a potential tool in neurodegeneration therapy of demyelination origin.

Moringa oleifera phytochemicals protect the brain against experimental nicotine-induced neurobehavioral disturbances and cerebellar degeneration.

Nicotine is a neuro-stimulant that has been implicated in the pathophysiology of many brain diseases. The need to prevent or alleviate the resulting dysfunction is therefore paramount, which has also given way to the use of medicinal plants in the management of brain conditions. This study was designed to determine the histomorphological and neurobehavioural changes in the cerebellum of Wistar rats following nicotine insult and how such injuries respond to Moringa intervention. Twenty-four adult male Wistar rats were divided into 4 groups. Group A and B were orally treated with normal saline and Moringa oleifera respectively for twenty-eight days; Group C was treated with nicotine while group D was treated orally with Moringa oleifera and intraperitoneally with nicotine for twenty-eight days. Animals were subjected to the open field test on the last day of treatment. 24 h after last day treatment, the animals were anesthetized and perfusion fixation was carried out. The cerebellum was excised and post-fixed in 4% paraformaldehyde and thereafter put through routine histological procedures. Results revealed cytoarchitectural distortion and extreme chromatolysis in neuronal cells of the cerebellar cortical layers in the nicotine-treated group. The Purkinje cells of the cerebellum of animals in this group were degenerated. There were also reduced locomotor activities in the group. Moringa was able to prevent the chromatolysis, distortion of the cerebellar cortical cells and neurobehavioural deficit. Our result suggests that Moringa oleifera could prevent nicotine-induced cerebellar injury in Wistar rats, with the possibility of ameliorating the clinical features presented in associated cerebellar pathology.

Moringa oleifera impairs the morphology and functions of the kidney in adult Wistar rats / Moringa oleifera altera la morfología y funciones del riñón en ratas Wistar adultas

We tested the hypothesis that Moringa oleifera impairs the morphology and functions of the kidney in rats. Twenty-four adult male Wistar rats were employed in the study. Rats of Control Group I received physiological saline while rats of Groups II ­ IV received 250, 500 and 750 mg/kg bodyweight of methanolic extract of Moringa oleifera respectively for twenty one days. No behavioral anomalies were observed in rats of Groups I ­ IV. Rats of Control Group I gained statistically significant increased bodyweight while rats of Groups II ­ IV experienced non-significant decreased bodyweight during experimental procedure. (P0.05). No statistical significant differences (P0.05) were observed in the analyses of the relative weights of kidneys of rats of Groups I ­ IV. Histological examinations showed normal cyto-architecture of the kidneys of rats of Group I while the Capsular spaces of the kidneys of rats of Groups II ­ IV appeared wider than those of Group I. Statistical analyses showed significant higher levels (P0.05) of Alanine and Aspartate Transaminases, and serum urea in rats of Groups II ­ IV in a non- dose-dependent manner when compared to rats of Group I. Our findings are consistent with the stated hypothesis.

Se puso a prueba la hipótesis que Moringa oleifera altera la morfología y función del riñón en ratas. Fueron utilizadas 24 ratas Wistar macho adultas. El grupo control recibió suero fisiológico mientras que los Grupos II a IV recibieron 250, 500 y 750 mg/kg peso corporal del extracto metanólico de Moringa oleifera respectivamente, durante 21 días. No se observaron anomalías en el comportamiento en ratas de los Grupos I - IV. En las ratas del grupo de control se registró un aumento de peso corporal estadísticamente significativo, mientras que las ratas de los grupos II - IV experimentaron una disminución no significativa de peso corporal durante el procedimiento experimental (P0,05). No se observaron diferencias estadísticamente significativas (P0,05) en el análisis de los pesos relativos en riñones de las ratas de los grupos I - IV. Los exámenes histológicos mostraron citoarquitectura normal de los riñones de las ratas del grupo I, mientras que en ratas de los grupos II ­ IV los espacios capsulares de los riñones aparecían más amplios que los del Grupo I. Los análisis estadísticos mostraron niveles superiores significativos ( P 0,05 ) de la alanina y aspartato aminotransferasa, y de urea en suero en ratas de los Grupos II - IV no dependiente de la dosis, en comparación con las ratas del Grupo I. Estos resultados coinciden con la hipótesis planteada.

Effects of combined leaf extract of Vernonia amygdalina and Azadirachta indica on hepatic morphology and hepatotoxicity markers in streptozotocin-induced diabetic rats.

OBJECTIVES: In this work, we studied liver morphology, markers of hepatic oxidative stress and some liver enzymes in diabetic rats treated with the combined leaf extract (CLE) of Vernonia amygdalina (bitter leaf) and Azadirachta indica (neem). METHODS: Diabetes was induced in fasted male Wistar rats with intraperitoneal injection of streptozotocin (STZ). Oral CLE (500 mg/kg body weight) and metformin (150 mg/kg body weight) were administered to different groups of diabetic rats for eight weeks. Blood glucose and change in body weight were estimated weekly. All animals were sacrificed under anaesthesia after eight weeks. Hepatic sections were stained with periodic acid-Schiff. Liver samples were homogenized and assayed for contents of malondialdehyde (MDA) and glutathione peroxidase (GPx), while the plasma was assayed for contents of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). RESULTS: Metformin and CLE treatment produced normoglycaemia in the diabetic rats in the course of the treatment period. Significant increases in body weight were observed in the treatment groups compared with the diabetic control rats (P<0.05). In the control and treatment groups, light microscopic study showed intact hepatic histology. Plasma ALT and AST were not significantly different from the control values in the CLE-treated rats. In addition, from week four onwards, blood glucose concentrations in the CLE-treated rats were not different from the normal control (P>0.05). Besides, hepatic MDA (P<0.05) significantly decreased in the CLE-treated rats compared with the normal control. CONCLUSION: These findings suggest that CLE ameliorates hyperglycemia and hepatic oxidative stress when administered to diabetic rats as a chronic regimen, and there was no morphologic or biochemical evidence of liver damage at the dose tested.