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Pterostilbene relieves mitochondrial oxidative damage in mice cerebral ischemia reperfusion model by activing heme oxygenase-1
Pages: 285-
292
Year: 2017
Issue:
3
Journal: Chinese Journal of Neuroanatomy
Abstract: Objective:To explore the effects of pterostilbene (PTE) on mitochondrial oxidative damage in mice cerebral ischemia reperfusion (IR) model and the possible mechanisms.Methods:IR injury was induced by bilateral common carotid arteries occlusion in mice using non-traumatic aneurysm clips.The mice received PTE or ZnPP,the inhibitor of heme oxygenase-1 (HO-1) by intraperitoneal injection.The mice were randomly divided into four groups:IR;PTE + IR;PTE + ZnPP + IR;ZnPP + IR.The dose of PTE used was 2.5 mg/kg,5 mg/kg and 10 mg/kg.The neurological scores were assessed and the brain edema was detected by wet-dried weight method.The sodium ion level in the brain was measured by flame photometry.The neuronal survival and the apoptotic ratio in IR-injured brains were detected by NeuN and TUNEL assay.The mitochondrial oxidative stress injury was evaluated through the measurements of mitochondrial membrane potential (MMP),reactive oxygen species (ROS) production,mitochondrial complex Ⅰ and Ⅳ activity.The protein expressions of HO-1,NADPH quinone oxidoreductase 1 (NQO1),glutathione s-transferases (GST),mitochondrial and cytosolic cytochrome c was detected by Western Blot.Results:PTE improved neurological scores of mice,low-ered brain edema and decreased the sodium ion content of brain.It up-regulated HO-1,NQO1 and GST expression.Moreover,PTE resulted in a well-preserved mitochondrial MMP,mitochondria complex Ⅰ/Ⅳ activity,mitochondrial cytochrome c level while it reduced mitochondrial ROS production and cytosolic cytochrome c level.However,the dosedependent PTE-elevated mitochondrial function was reversed by ZnPP.Conclusion:In mice cerebral IR model,PTE plays a role in the brain protection by reducing mitochondrial oxidative damage and cell death through the activation of HO-1 signal.
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