Licorice extract attenuates brain aging of d-galactose induced rats through inhibition of oxidative stress and attenuation of neuronal apoptosis

Abstract

Licorice, an edible and officinal plant, has attracted considerable attention for its wide range of pharmacological activities. The present study focused on the protective effect of licorice on aging rats and on exploring its potential mechanisms. Aging in rats was induced by D-gal (300 mg kg⁻¹) for 5 weeks continuously with intraperitoneal injection, while control rats received physiological saline, and other groups received different concentrations of licorice extract (1, 5 and 10 g of herb per kg) by oral gavage after being D-gal induced. Their spatial and learning memory abilities were evaluated by the Morris water maze test and an object-place recognition test. Some related biochemical indices were also determined by assay kits. Neuronal cell injury in the hippocampal region was observed by hematoxylin and eosin (HE) staining. The expression levels of Bax, Bcl-2, caspase-3 and Cyt-C in the hippocampus were detected by western blot. The results showed that licorice extract could significantly ameliorate the learning and memory abilities impaired by D-gal. The licorice extract significantly increased the SOD, GSH-Px and CAT activity and synchronously decreased the content of MDA in the hippocampus. It also ameliorated the dysfunction of the cholinergic system induced by D-gal. Furthermore, the licorice extract also protected the hippocampal neurons against damage and could significantly reduce the expression of the Bax/Bcl-2 protein ratio, caspase-3 and Cyt-C protein in the hippocampus. These findings indicate that the licorice extract effectively attenuated cognitive damage, improved oxidative stress and apoptosis in aging rats induced by D-gal, and played a significant role in antioxidation and anti-neuronal apoptosis.