Aging is an inevitable biological process characterized by motor in coordination and decline in the ability to learn new motor skills. The purpose of this study is to investigate, for the first time, the beneficial antiaging effects of medical ozone (O3) on the age-related structural damage of the rat cerebellum. We have examined the cerebellum of albino rats at the ages of 6, 20 and 22, and the effect of intraperitoneal medical O3 administration (0.7 g/kg) by histological, immunohistochemical and morphometric studies. Age-related changes in the cerebellum were in the form of a significant reduction in the number of Purkinje cells (PCs), which appeared shrunken with a darkly stained cytoplasm and vacuolated spaces in all layers. The decrease in Nissl granule content of the PCs was also observed. A significant reduction in Mab2, Ki67 immunoreactivity associated with significant increase in glial fibrillary acidic protein, Caspase-3 and iNos immunoreactivity were also detected. Medical O3 administration reversed all these histopathological and immunohistochemical changes. This protective effect was mediated by reducing oxidative stress, apoptosis, astrocyte activation and improving both neuritogenesis and neurogenesis. We can conclude from the results of the present study that medical O3 can prevent the retardation of age-related changes in rat cerebellum.
Background
Atherosclerosis is a major cardiovascular disease and one of the commonest causes of mortality in the world. Speech, balance, fine motor control and cognition are affected by atherosclerosis of cerebellar arteries. This study investigated the protective role of vitamin E against induced atherosclerosis in the rabbit cerebellum.
Materials and methods
Forty Rex New Zealand adult male rabbits were randomly divided into four groups (10 rabbits each). Group I was designated as the control and received an ordinary diet. Group II received an ordinary diet, but with vitamin E (12 mg/kg/day) added. Group III were given an ordinary diet along with 1% cholesterol powder for 6 weeks. Finally, group IV received an ordinary diet with both 1% cholesterol powder and vitamin E (12 mg/kg/day). Cerebellum samples were stained with haematoxylin and eosin and examined using light microscopy, along with quantitative immunohistochemical assessments of the expression of caspase-3, glial fibrillary acidic protein (GFAP) and inducible nitric oxide synthase (iNOS).
Results
Cerebellum sections from cholesterol-treated rabbits showed ischaemic changes as fibre density decreased, with vacuolation of the molecular layer, and deformed and shrunken Purkinje cells. A significant increase in caspase-3, GFAP and iNOS immunoreactivity was found. However, vitamin E administration reduced these ischaemic manifestations.
Conclusions
The results demonstrate the neurological protective role of vitamin E therapy in atherosclerosis.
Objectives: Fluoride is a toxic and reactive element. Human beings are exposed to fluoride from various sources such as toothpastes, mouth rinses, dietary supplements and ordinary drinking water. This work investigated the effect of sodium fluoride (NaF), alone or with green tea, on the grey matter of spinal cord of adult male albino rats.
Methods:Spinal cord sections were examined using light and electron microscopy. Immunohistochemical assessments for the expression of caspase-3 and glial fibrillary acidic protein were performed. Agarose gel electrophoresis was used for DNA fragmentation.
Results:Our results showed that NaF produced neurodegeneration, vacuolation and haemorrhage with some abnormal blood vessels and a significant increase in the number and size of astrocytes. In addition, the neurons showed a significant decrease of their Nissl's granules content and significant increased expression of caspase-3.
Conclusion:Green tea exerted a protective effect against NaF-induced neurotoxicity. The results of this work add to the known toxic effects of NaF and provide a new insight into the possible use of green tea to ameliorate these effects.
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