| First Author | Dai Y | Year | 2020 |
| Journal | Front Cell Dev Biol | Volume | 8 |
| Pages | 593659 | PubMed ID | 33330477 |
| Mgi Jnum | J:342995 | Mgi Id | MGI:6729484 |
| Doi | 10.3389/fcell.2020.593659 | Citation | Dai Y, et al. (2020) Echinacoside Suppresses Amyloidogenesis and Modulates F-actin Remodeling by Targeting the ER Stress Sensor PERK in a Mouse Model of Alzheimer's Disease. Front Cell Dev Biol 8:593659 |
| abstractText | Endoplasmic reticulum stress (ERS) plays a vital and pathogenic role in the onset and progression of Alzheimer's disease (AD). Phosphorylation of PKR-like endoplasmic reticulum kinase (PERK) induced by ERS depresses the interaction between actin-binding protein filamin-A (FLNA) and PERK, which promotes F-actin accumulation and reduces ER-plasma membrane (PM) communication. Echinacoside (ECH), a pharmacologically active component purified from Cistanche tubulosa, exhibits multiple neuroprotective activities, but the effects of ECH on ERS and F-actin remodeling remain elusive. Here, we found ECH could inhibit the phosphorylation of PERK. Firstly ECH can promote PERK-FLNA combination and modulate F-actin remodeling. Secondly, ECH dramatically decreased cerebral Abeta production and accumulation by inhibiting the translation of BACE1, and significantly ameliorated memory impairment in 2 x Tg-AD mice. Furthermore, ECH exhibited high affinity to either mouse PERK or human PERK. These findings provide novel insights into the neuroprotective actions of ECH against AD, indicating that ECH is a potential therapeutic agent for halting and preventing the progression of AD. |
