Neuroprotective and anti-neuroinflammatory effects of ethanolic extract from leaves and stems of Aster glehni

[Display omitted] •EAG showed neuroprotective effects in SH-SY5Y cells with Aβ.•EAG suppressed Aβ-induced neurotoxicity via ERK-CREB-BDNF signaling pathway.•EAG alleviated neuroinflammation related to NF-κB pathway in BV-2 cells.•EAG could be used as a preventive and therapeutic agent for neurodegenerative diseases. Aster glehni Fr. Schm. has been reported ameliorating effects on cognitive dysfunction. However, the molecular mechanisms underlying neurodegenerative diseases such as Alzheimer’s disease (AD) are poorly understood. Herein, we examined whether the ethanolic extract from leaves and stems of Aster glehni Fr. Schm. (EAG) could have biological effects for therapy-related AD. EAG exerted the neuroprotective effects in SH-SY5Y neuroblastoma cells through extracellular signal-regulated kinase (ERK)/cAMP response element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF) pathway. In addition, EAG suppressed expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and productions of nitric oxide (NO), and pro-inflammatory cytokines by blocking nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. This study also investigated that EAG possessed anti-neuroinflammatory effects in scopolamine-induced mice. Taken together, EAG and its caffeoylquinic acid could have anti-neurodegenerative properties derived from its ability to induce neuroprotection and anti-neuroinflammation.