title: Ginsenoside Rg1 prevents SK-N-SH neuroblastoma cell apoptosis induced by supernatant from Aβ1-40-stimulated THP-1 monocytes.
abstract: Excessive accumulation of amyloid-β (Aβ) has been proposed as a pivotal event in Alzheimer's disease (AD) pathogenesis. Possible mechanisms underlying Aβ-induced neurotoxicity include inflammation and apoptosis. Here, the protective effect of ginsenoside Rg1 (GRg1) on neuronal damage was examined in an in vitro inflammatory neurodegeneration model. Supernatant from Aβ(1-40)-stimulated THP-1 monocytes was added to SK-N-SH neuroblastoma cell culture medium. Incubation of SK-N-SH cells with cell-free supernatant from Aβ(1-40) (125nM)-treated THP-1 monocytes for 24 h significantly increased lactate dehydrogenase (LDH) release, cell apoptosis, Bax and caspase-3 expression in SK-N-SH cells. However, pretreating THP-1 monocytes with GRg1 (50, 100 or 150 μM) for 30 min markedly reduced IL-1β, IL-8 and TNF-α levels in Aβ(1-40)-stimulated supernatant. LDH release, cell apoptosis, Bax and caspase-3 expression in SK-N-SH cells were significantly decreased when cultured with cell-free supernatant from Aβ(1-40)-stimulated THP-1 monocytes that were pretreated with GRg1. The results suggest that Aβ(1-40)-induced neuronal injury and apoptosis may be mediated by inflammatory monocyte reactions, and GRg1 exerts a protective effect against Aβ(1-40)-induced neuronal injury and apoptosis, likely through its anti-inflammatory mechanism.
authors.affiliation: Department of Neurology, Henan Provincial People's Hospital, Zhengzhou, Henan Province 450003, PR China.
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Yanqi
authors.initials: Y
authors.lastname: Chu
authors.forename: Lan
authors.initials: L
authors.lastname: Zhang
authors.forename: Linlin
authors.initials: L
authors.lastname: Yin
authors.forename: Lin
authors.initials: L
authors.lastname: Li
mesh_terms: D016229:Amyloid beta-Peptides / Q000037:antagonists & inhibitors / Q000633:toxicity*; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D002457:Cell Extracts; D002460:Cell Line; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D002474:Cell-Free System / Q000502:physiology; D019610:Cytoprotection / Q000187:drug effects / Q000502:physiology*; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D036145:Ginsenosides / Q000502:physiology* / Q000627:therapeutic use; D006801:Humans; D009000:Monocytes / Q000187:drug effects / Q000502:physiology*; D009447:Neuroblastoma / Q000378:metabolism / Q000473:pathology*; D010446:Peptide Fragments / Q000037:antagonists & inhibitors / Q000633:toxicity*
chemical_list: D016229:Amyloid beta-Peptides; D000893:Anti-Inflammatory Agents; D002457:Cell Extracts; D004365:Drugs, Chinese Herbal; D036145:Ginsenosides; D010446:Peptide Fragments; C078592:amyloid beta-protein (1-40); C035054:ginsenoside Rg1