Cyanidin 3-O-β-Galactoside Alleviated Cognitive Impairment in Mice by Regulating Brain Energy Metabolism During Aging.

Abstract

Metabolic disorder, which commonly happens among senile people worldwide, is an important sign of aging. The early symptoms of neurodegenerative diseases include a decrease in energy metabolism and mitochondrial dysfunction. Comparably, early dietary intervention may be more effective in preventing or delaying brain aging, owing to its role in regulating metabolism. Polyphenol intake has shown its potential in preventing Alzheimer's disease. However, whether there are close connections between polyphenols and the energy metabolism of the brain during aging remains unclear. This study sought to evaluate whether cyanidin 3-O-β-galactoside from black chokeberry (Aronia melanocarpa (Michx.) Elliott) has positive effects on energy metabolism, as well as cognitive function in aging mice. Intragastrical administration of cyanidin 3-O-β-galactoside (25 and 50 mg/kg/day) for 8 weeks effectively alleviated the decline in brain glucose uptake (decline rate 18.29% versus 1.05%, 7.63%) of aging mice. Moreover, cyanidin 3-O-β-galactoside also alleviated neuronal damage in the hippocampus (number of neurons 212.33 ± 16.19 versus 285.33 ± 29.53, 301.67 ± 10.07; p < 0.05) and cortex (number of neurons 82.00 ± 4.58 versus 111.67 ± 6.51, 112.00 ± 1.00; p < 0.05). Furthermore, cyanidin 3-O-β-galactoside reduced β-amyloid load in the brain and significantly increased the crossing-platform number (0.92 ± 1.11 versus 1.83 ± 0.68, 2.08 ± 0.58; p < 0.05) in the Morris water maze test. We further determined that protein kinase B (AKT) might be the target of cyanidin 3-O-β-galactoside, which played a beneficial role in controlling the energy metabolism of the brain. These results suggested that early intervention of anthocyanins could promote neuroprotection under the challenge of brain energy metabolism.