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.
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