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چکیده:  
Introduction: This study was aimed at assessing the protective mechanisms of Kolaviron on the cerebellum in a rat model of demyelination.
Methods: Twenty-eight male Wistar rats were used for the study. They were categorised into 4 groups and each group had 7 rats each. Group A (control) received corn oil (0.5 ml/kg/day), Group B received 0.2% cuprizone, Group C was treated with Kolaviron (200 mg/kg/day), while Group D received 0.2% cuprizone and Kolaviron (200 mg/kg/day), for 6 weeks. Behavioural test was conducted following treatments; cerebellar homogenate was obtained for spectrophotometric assays of oxidative stress parameters, and brain tissue was processed for histolochemical and immunohistochemical studies.
Results: Data showed no significant weight gain and reduced exploratory activities in cuprizone (CPZ)-treated rats. The neurons were characterized with cryptic granules, chromatolytic, pyknotic Purkinje cell bodies with short dendritic and axonal processes and layers that were not well demarcated. These correlate with observable hypertrophic astrogliosis, depleted antioxidant system shown by decreased level of superoxide dismutase, glutathione peroxidase and elevated malondialdehyde level.
Conclusion: Kv protects the cerebellar degeneration through the regulation of stress-related markers and signaling pathways implicated in demyelination. Cellular, molecular and behavioural alterations are associated with CPZ-induced demyelination, while Kv significantly inhibits corresponding neurotoxicity making it a potential candidate for treating demyelinating diseases.
نوع مطالعه: Original | موضوع مقاله: Cellular and molecular Neuroscience
دریافت: ۱۳۹۷/۱/۱ | پذیرش: ۱۳۹۷/۹/۶ | انتشار: ۱۳۹۷/۹/۷

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