Emodin is a naturally‑occurring medicinal herbal ingredient that possesses numerous pharmacological properties, including anti‑inflammatory and antioxidant effects. In the present study, potential neuroprotective effects associated with the antioxidant activity of emodin were assessed in U251 cells that were subjected to β‑amyloid peptide (Aβ)‑induced apoptosis and in amyloid precursor protein (APP)/presenilin‑1 (PS1) double‑transgenic mice. U251 is a type of human astroglioma cell line (cat. no. BNCC337874; BeNa Culture Collection). In apoptotic U251 cells, 3‑h emodin pre‑treatment prior to 24‑h Aβ co‑exposure improved cell viability, suppressed lactate dehydrogenase leakage and caspase‑3, ‑8 and ‑9 activation to inhibit apoptosis. Compared with those after Aβ exposure alone, emodin ameliorated the dissipation of the mitochondrial membrane potential, inhibited the over‑accumulation of reactive oxygen species, enhanced the expression levels of nuclear factor‑erythroid‑2‑related factor 2 (Nrf2), haemeoxygenase‑1, superoxide dismutase 1, Bcl‑2 and catalase in addition to decreasing the expression levels of Bax. In APP/PS1 mice, an 8‑week course of emodin administration improved spatial memory and learning ability and decreased anxiety. Emodin was also found to regulate key components in the Nrf2 pathway and decreased the deposition of Aβ, phosphorylated‑τ and 4‑hydroxy‑2‑nonenal in APP/PS1 mice. Taken together, the present data suggest that emodin may serve as a promising candidate for the treatment of Alzheimer's disease.
Keywords: emodin; Alzheimer's disease; β‑amyloid peptide; nuclear factor‑erythroid‑2‑related factor 2; oxidative stress.