Abstract
The interruption of hippocampal neurogenesis due to aging impairs memory. The accumulation of D-galactose (D-gal), a monosaccharide, induces brain aging by causing oxidative stress and inflammation, resulting in neuronal cell damage and memory loss. Chrysin, an extracted flavonoid, has neuroprotective effects on memory. The present study aimed to investigate the effect of chrysin on memory and hippocampal neurogenesis in brains aged using D-gal. Male Sprague-Dawley rats received either D-gal (50 mg/kg) by i.p. injection, chrysin (10 or 30 mg/kg) by oral gavage, or D-gal (50 mg/kg) and chrysin (10 or 30 mg/kg) for 8 weeks. Memory was evaluated using novel object location (NOL) and novel object recognition (NOR) tests. Hippocampal neurogenesis was evaluated using Ki-67, 5-bromo-2′-deoxyuridine (BrdU), and doublecortin (DCX) immunofluorescence staining to determine cell proliferation, cell survival, and number of immature neurons, respectively. We found that D-gal administration resulted in memory impairment as measured by NOL and NOR tests and in depletions in cell proliferation, cell survival, and immature neurons. However, co-treatment with chrysin (10 or 30 mg/kg) attenuated these impairments. These results suggest that chrysin could potentially minimize memory and hippocampal neurogenesis depletions brought on by aging.
Highlights
Self-renewal is an important property of neural stem cells (NSCs) in neurogenic niches including the subventricular zone (SVZ) and the subgranular zone (SGZ)
This study showed no differences in locomotor activity after receiving D-gal and chrysin
The animals in the vehicle, chrysin 10, chrysin 30, and D-gal + chrysin groups spent significantly longer exploring the object in the novel location than that in the familiar location (* p < 0.05, Figure 1B), but this was not observed in the D-gal group (p > 0.05, Figure 1B)
Summary
Self-renewal is an important property of neural stem cells (NSCs) in neurogenic niches including the subventricular zone (SVZ) and the subgranular zone (SGZ). This phenomenon is potentially important in neurogenesis [1]. Generated neurons in the SGZ of hippocampal dentate gyrus (DG) are connected to the existing hippocampal circuit and play a role in memory [2,3]. The biomolecular mechanism of aging is associated with homeostasis disruption, which causes cell death [6]. Disturbing neurogenesis in the SGZ causes memory impairment which is a major problem in brain aging [7,8]
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