The Protective Effect Of Kamperol On Focal Cerebral Ischemia In Rats

BackgroundIrreversible brain disorder usually comes occur due to the ischemical reperfusion injury. A large amount of basic and clinical researches had been made for, but there has no breakthrough progress comes still. The study of molecular biology demonstrated that multiple factors involved in the process of cerebral ischemia reperfusion injury, apoptosis, free radical damage, calcium overload, excitotoxicity of amino acids and others have been validated by most experiments. The death of nerve cell after brain injury can be divided into two types: cellular necrosis and apoptosis, which play a key role in secondary injury. The primary injury is unavoidable, so to block nerve cell apoptosis in the secondary injury in early stage become the important turning point in the protection ofbrain injury.Aim: To investigate whether kaempferol exerts a neuroprotective effect on focal cerebral ischemia in normotensive rats.Methods: The model of focal cerebral ischemia in rats was established by middle cerebral artery occlusion (MCAO) for 90 min followed by perfusion. Rats are randomly divided into sham-operated group, focal cerebral ischemia group, kaempferol-treating (10mg/kg) groups, and positive control (Edaravone-treating) group. Rats were killed and brain samples were collected for the measurement of infarct size and the content of super oxide dismutase, glutathione peroxidase (GSH-Px), nitric oxide, malondialdehyde (MDA). Furthermore, the expression of activated Caspase-3 were evaluated with immunohistochemitry and the apoptosis of neurons were determined by deoxynucleodyltransferase-mediated biotinylated UTP nick end labeling (TUNEL).Results: Kaempferol could significantly increase the activities of SOD, GSH-px, the content of nitric oxide, and decrease the content of MDA in the cerebral ischemia reinfusion model of rats. Meanwhile, kaempferol treatment obviously decreased the number of TUNEL-positive cells and the expression of activated caspase-3 in the penumbra.Conclusion: Kaempferol exhibits neuroprotection against transient cerebral ischemia. The neuroprotective effects in ischemic tissue may be associated with reducing free radicals and its inhibition of apoptotic cell death in the penumbra.