Ginsenoside Rg1 prevents SK-N-SH neuroblastoma cell apoptosis induced by supernatant from Aβ1–40-stimulated THP-1 monocytes

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 Aβ1–40-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 Aβ1–40 (125 nM)-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 Aβ1–40-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 Aβ1–40-stimulated THP-1 monocytes that were pretreated with GRg1. The results suggest that Aβ1–40-induced neuronal injury and apoptosis may be mediated by inflammatory monocyte reactions, and GRg1 exerts a protective effect against Aβ1–40-induced neuronal injury and apoptosis, likely through its anti-inflammatory mechanism.

► The protective effect of GRg1 was examined in a new in vitro model.
► Supernatant from Aβ1–40-stimulated THP-1 was added to neuronal culture medium.
► Incubation of SK-N-SH with supernatant from THP-1 increased cell apoptosis.
► Pretreating THP-1 cells with GRg1 for 30 min prevented cell apoptosis.
► GRg1 may exert protective effect through its anti-inflammatory mechanism.