Abstract
Arctigenin (Arc) has been shown to act on scopolamine-induced memory deficit mice and to provide a neuroprotective effect on cultured cortical neurons from glutamate-induced neurodegeneration through mechanisms not completely defined. Here, we investigated the neuroprotective effect of Arc on H89-induced cell damage and its potential mechanisms in mouse cortical neurons and human SH-SY5Y neuroblastoma cells. We found that Arc prevented cell viability loss induced by H89 in human SH-SY5Y cells. Moreover, Arc reduced intracellular beta amyloid (Aβ) production induced by H89 in neurons and human SH-SY5Y cells, and Arc also inhibited the presenilin 1(PS1) protein level in neurons. In addition, neural apoptosis in both types of cells, inhibition of neurite outgrowth in human SH-SY5Y cells and reduction of synaptic marker synaptophysin (SYN) expression in neurons were also observed after H89 exposure. All these effects induced by H89 were markedly reversed by Arc treatment. Arc also significantly attenuated downregulation of the phosphorylation of CREB (p-CREB) induced by H89, which may contribute to the neuroprotective effects of Arc. These results demonstrated that Arc exerted the ability to protect neurons and SH-SY5Y cells against H89-induced cell injury via upregulation of p-CREB.
Highlights
Arctigenin (Arc) is the main active constituent that is extracted and isolated from the fruit of Arctium lappa L., which has been used as an herbal medicine for its antipyretic and anti-inflammatory actions
To investigate whether Arc could rescue the loss of cell viability, human SH-SY5Y cells were treated with H89 (50 μM, 1 h) before being incubated with Arc (0.25–10 μM for 24 h)
We found that Arc treatment could inhibit H89-induced depression of cell viability and neural apoptosis in both types of cells, thereby rescuing them from neurodegeneration and confirming the neuroprotective action of Arc against H89
Summary
Arctigenin (Arc) is the main active constituent that is extracted and isolated from the fruit of Arctium lappa L., which has been used as an herbal medicine for its antipyretic and anti-inflammatory actions. Arc exerts a neuroprotective effect on both glutamate-induced neurotoxicity in primary neurons and scopolamine-induced learning and memory deficits in mice with Alzheimer’s disease (AD) [4,5]. Activation of CREB is essential for the formation and retention of memory, which is the main physiological parameter of Alzheimer’s disease [8]. The process of CREB activation is considered to be a major mechanism in the promotion of neuronal growth and survival [9]. Reduced phosphorylation of CREB (p-CREB), which is considered to be one of the consequences of Aβ-induced neurotoxicity, has been observed in the postmortem brains of AD patients, Aβ-treated neurons [10] and in Tg-AD mice that overexpress. We used H89 to induce neural cell damage via downregulation of p-CREB [19,20] and investigated if Arc protects neural cells against CREB inactivation
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