Ginsenoside Rg1 prevents SK-N-SH neuroblastoma cell apoptosis induced by supernatant from A尾_1-40-stimulated THP-1 monocytes

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• 作者：Wei Li^a ; Yanqi Chu^b ; Lan Zhang^b ; Linlin Yin^b ; Lin Li^b ; ^{linli97@hotmail.com}
• 关键词：Ginsenoside Rg1 ; Amyloid-尾1&ndash ; 40 ; THP-1 monocytes ; SK-N-SH neuroblastoma cells ; Cell viability ; Apoptosis ; Inflammation
• 刊名：Brain Research Bulletin
• 出版年：2012
• 期刊代码：9_03619230
• 类别：neu
• 出版时间：1 August, 2012
• 卷：88
• 期：5
• 页码：501-506
• 文件大小：709 K

摘要

Excessive accumulation of amyloid-尾 (A尾) has been proposed as a pivotal event in Alzheimer's disease (AD) pathogenesis. Possible mechanisms underlying A尾-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 A尾_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 A尾_1-40 (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 渭M) for 30 min markedly reduced IL-1尾, IL-8 and TNF-伪 levels in A尾_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 A尾_1-40-stimulated THP-1 monocytes that were pretreated with GRg1. The results suggest that A尾_1-40-induced neuronal injury and apoptosis may be mediated by inflammatory monocyte reactions, and GRg1 exerts a protective effect against A尾_1-40-induced neuronal injury and apoptosis, likely through its anti-inflammatory mechanism.