Cerebral ischemia reperfusion (IR) injury as found in stroke is a complex and heterogeneous disorder and closely related to disability and death. Today, nutraceuticals and protective therapy to increase neuronal integrity and prevent pathological complication are common. We investigated the neuroprotective effect of betanin against cerebral IR injury in mice. Forty male institute of cancer research (ICR) mice were divided into Sham-veh, IRveh, IR-Bet50 and IR-Bet100 groups. After 2 weeks of oral administration of normal saline (vehicle; veh) or 50 mg/kg or 100 mg/kg of betanin (Bet), mice were subjected to IR induction using 30-min bilateral common carotid artery occlusion, followed by 24 hrs. of reperfusion. Brain infarction, oxidative status, cortical and hippocampal neurons and white matter pathologies were evaluated. Results showed that IR significantly increases brain infarction, Cornus Ammonis 1 (CA1) hippocampal and corpus callosum (CC) and internal capsule (IC) white matter degeneration (p < 0.05). Brain oxidative status revealed significant elevation of malondialdehyde (MDA) together with a significant decrease in catalase (CAT) activity, induced by IR (p < 0.05). Pretreatment with betanin 100 mg/kg led to a significant reduction in brain infarction and MDA, CA1 hippocampus, CC and IC white matter degeneration. Betanin also led to a significant increase in CAT activity (p < 0.05), with enhancing effect on reduced glutathione levels (GSH, p < 0.05). The present study revealed the neuroprotective efficacy of betanin against IR injury in mice's brains, including its inhibition of lipid peroxidation, and boosting of GSH and CAT activity.

Cerebral ischemia reperfusion (IR) injury as found in stroke is a complex and heterogeneous disorder and closely related to disability and death. Transient ischemia causes energy deprivation and leads to failure of neuronal function. Recirculation complications also facilitate acute and delayed neuronal death as well as white matter injury. Today, nutraceuticals and protective therapy to increase neuronal integrity and prevent pathological complication are common. We investigated the neuroprotective effect of betanin against cerebral IR injury in mice. We randomly divided forty male ICR mice into Sham-veh, IR-veh, IR-Bet50 and IR-Bet100 groups. After 2 weeks of oral administration of normal saline (veh) or 50 mg/kg or 100 mg/kg of betanin, we subjected the mice to IR induction using 30-min bilateral common carotid artery occlusion, followed by 24 hrs. of reperfusion. We sacrificed the mice to evaluate brain infarction, brain oxidative status, cortical and hippocampal neurons and white matter pathologies. The results showed that IR significantly increases brain infarction, CA1 hippocampal degeneration and corpus callosum (CC) and internal capsule (IC) white matter loss (p < 0.05). Evaluation of brain oxidative status revealed significant elevation of malondialdehyde (MDA) together with a significant decrease in catalase (CAT) activity, induced by IR (p < 0.05). Pretreatment with betanin, especially a dose of 100 mg/kg, led to a significant reduction in brain infarction and MDA, CA1 hippocampus, CC and IC white matter degeneration. Betanin also led to a significant increase in CAT activity (p < 0.05), with enhancing effect on reduced glutathione levels (GSH, p < 0.05). Corroborating this finding, the present study revealed the neuroprotective efficacy of betanin against IR injury in mice’s brains. These effects were associated with betanin’s potent antioxidative properties, including its inhibition of lipid peroxidation, indicated by MDA attenuation, and boosting of GSH and CAT activity.