Neuroprotective effects of liquiritin on cognitive deficits induced by soluble amyloid-β1–42 oligomers injected into the hippocampus

Abstract

This study assessed the modulating effects of liquiritin against cognitive deficits, oxidative damage, and neuronal apoptosis induced by subsequent bilateral intrahippocampal injections of aggregated amyloid-β1–42 (Aβ1–42). This study also explored the molecular mechanisms underlying the above phenomena. Liquiritin was orally administered to rats with Aβ1–42-induced cognitive deficits for 2 weeks. The protective effects of liquiritin on the learning and memory impairment induced by Aβ1–42 were examined in vivo by using Morris water maze. The rats were then euthanized for further studies. The antioxidant activities of liquiritin in the hippocampus of the rats were investigated by biochemical and immunohistochemical methods. The apoptosis of the neurons was assessed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling assay. Liquiritin at doses of 50–100 mg/kg significantly improved the cognitive ability, restored the abnormal activities of glutathione peroxidase and superoxide dismutase, and decreased the levels of malondialdehyde，8-hydroxy-2′-deoxyguanosine and protein carbonyl in the hippocampus of rats with Alzheimer’s disease. Moreover, neural apoptosis in the hippocampus of Aβ1–42-treated rats was reversed by liquiritin. Liquiritin can significantly ameliorate Aβ1–42-induced spatial learning and memory impairment by inhibiting oxidative stress and neural apoptosis.