Chrysin alleviates the impeded neurogenesis in accelerated brain aging by D-galactose in rats.

Abstract

Aged-related cognitive impairments are associated with molecular neurodegenerations and impeded neurogenesis in the dentate gyrus (DG) of the damaged hippocampus. Neurogenesis requires activated cyclic AMP-responsive element-binding protein (CREB) pathway to enhance neuronal development, synaptic plasticity, cognition, learning and memory. Current research has reported that consecutive administration of D-galactose can accelerate brain aging by inducing oxidation and inflammation. The flavonoid chrysin has been demonstrated in medical dietary supplements and shown neuroprotective effect on impeded neurogenesis. This study aimed to clarify that chrysin preserves neurogenesis by modulating molecular pathway in accelerated brain aging induced by D-galactose. Signs of aging, processes of neurogenesis, and protein regulating neurogenesis were evaluated in male Sprague Dawley (SD) rats, which were allocated into four groups: vehicle rats, accelerated aging rats treated with D-galactose, normal rats receiving chrysin, and cotreated rats receiving both D-galactose and chrysin. Aging signs showed only a subsidence in volume of the granular cell layer (GCL) after consecutive administration of D-galactose. Cell proliferation, neurogenic niches, and protein regulating proliferation were downregulated in the accelerated aging rats. Likewise, cell survivals and proteins related to CREB pathway were depleted in rats receiving D-galactose. Nevertheless, rats cotreated with chrysin maintained in all parameters that were adversely affected by D-galactose. In conclusion, chrysin could alleviate the disruption of molecular regulation of neurogenesis in accelerated brain aging induced by D-galactose.