Beta Amyloid Peptide: Research Paper : Neuroprotective effect of emodin against Alzheimer's disease via Nrf2 signaling in U251 cells and APP/PS1 mice

Neuroprotective effect of emodin against Alzheimer's disease via Nrf2 signaling in U251 cells and APP/PS1 mice

Abstract

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

This article originally appeared in the "https://pubmed.ncbi.nlm.nih.gov/33300068/" and has their copyrights. We do not claim copyright on the content. This information is for research purposes only. This Blog is made available by publishers for educational purposes only as well as to give you general information and a general understanding , not to provide specific advice. By using this blog site you understand that there is no client relationship between you and the Blog publisher. The Blog should not be used as a substitute for competent research advice.