Auraptene and Other Prenyloxyphenylpropanoids Suppress Microglial Activation and Dopaminergic Neuronal Cell Death in a Lipopolysaccharide-Induced Model of Parkinson’s Disease
Vascular dementia and Alzheimer disease are most common type of dementia. These diseases have been associated with cognitive decline and affected personal behavioral activities. Moreover, the pattern of cerebral blood flow in mild cognitive disorder has appeared as a predictive indication for the development into Alzheimer's disease. Permanent, bilateral occlusion of the common carotid arteries (2VO) is a standard animal model to study vascular dementia and chronic cerebral hypoperfusion. In present study neuroprotective and memory enhancing effects of auraptene (AUR), a citrus coumarin, were studied in 2VO rats. Different doses (25, 8 & 4mg/kg) of AUR were administered orally. The spatial memory performance was tested with Morris water maze after 2VO induction. Biochemical experiments and histopathological evaluations were also applied to investigate the neuroprotective effect of AUR in brain tissue. In comparison with 2VO group, AUR could significantly decrease the scape latency time in treated rats. Also AUR increased the percentage of time spent and traveled pathway in target quadrant on final trial test day. All behavioral results were confirmed by biochemical and histopathological data. Biochemical data indicated that AUR could decrease malondialdehyde (MDA), as lipid peroxidation indicator, and increase glutathione (GSH) content in cortex and hippocampus tissues. Histopathological data showed that AUR could protect cerebrocortical and hippocampus neurons against ischemia. This study demonstrated the memory enhancing effect and neuroprotective activity of AUR after induction of brain ischemia in a rat model of vascular dementia.