Evaluating the Protective Effect of Ginsenoside Re on Hippocampal Mitochondria in a Rat Model of Vascular Dementia

Abstract

Vascular dementia (VD) is a common disease among elderly individuals that results in cognitive dysfunction. Although pharmaceutical treatments are used to temporarily improve the symptoms, these have side effects, including mental disorders and epilepsy. Therefore, identifying therapeutic strategies for VD which limit side effects would be advantageous. Previous studies have demonstrated the involvement of oxidative stress in the pathogenesis of VD. As the major saponin type of Panax ginseng, Ginsenoside Re, exerts anti-oxidation and anti-inflammation effects, Re may have a therapeutic role in the management of VD. Our aim was to evaluate this potential therapeutic role of Re in a rat model of VD. We compared mitochondrial function in hippocampal neurons in groups with or without Re administration. Our findings show that Re administration can reverse the effects of VD on mitochondrial structure and function in hippocampal neurons, including protecting against a reduction in the number of mitochondria and preventing mitochondrial vacuolization. The relative expression levels of COX IV and PDH-A1 also increased after Re treatment, with a reduction in mitochondrial H2O2 production, in a time-and dose-dependent manner. These improvements in mitochondrial function protected against VD-associated cognitive dysfunction, measured by performance in a Morris water maze. Based on these findings, we concluded that Ginsenoside Re may ameliorate cognitive impairment in VD by inhibiting mitochondrial oxidative stress in the brain. Collectively, we provide valuable experimental data which could inform the development of safe and effective drugs for the management of VD from ischemia.