Salidroside protects PC12 cells from Aβ1‑40‑induced cytotoxicity by regulating the nicotinamide phosphoribosyltransferase signaling pathway.
Salidroside protects PC12 cells from Aβ1‑40‑induced cytotoxicity by regulating the nicotinamide phosphoribosyltransferase signaling pathway.
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Salidroside 通过调节烟酰胺磷酸核糖基转移酶信号通路保护 PC12 细胞免受 A beta(1-40) 诱导的细胞毒性
DOI：
10.3892/mmr.2017.6931
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发表时间：
2017-09
影响因子：
3.4
通讯作者：
Chen J
中科院分区：
文献类型：
--
作者：
Huang X;Xing S;Chen C;Yu Z;Chen J
阿尔茨海默病（Alzheimer's disease，AD）是最常见的老年性痴呆，常发生于老年人或早老个体。淀粉样β蛋白（amyloid β-protein，Aβ）作为AD的病理特征之一，可引起能量代谢异常，从而导致细胞损伤和凋亡。红景天苷是中药红景天的主要活性成分。先前的研究表明红景天苷在能量代谢中发挥调节作用。然而，红景天苷在AD中的作用和作用机制仍不清楚。因此，本研究利用Aβ1-40诱导PC 12细胞损伤，从而建立AD细胞模型。此外，通过红景天苷处理来研究红景天苷的保护作用及其机制。Aβ1-40诱导的神经元毒性降低了细胞活力并导致细胞损伤。结果，烟酰胺磷酸核糖基转移酶（NAMPT）的表达水平降低，烟酰胺腺嘌呤二核苷酸（NAD+;能量代谢相关辅酶）的合成变得不足，并且NAD+/烟酰胺腺嘌呤二核苷酸氢化物比率降低。红景天苷可减轻Aβ诱导的细胞损伤，增加关键蛋白NAMPT的表达和NAD+的合成。本研究结果表明红景天苷对Aβ1-40损伤的PC 12细胞具有保护作用。其潜在机制可能与能量代谢的调节有关，主要依赖于NAMPT信号通路。
Alzheimer's disease (AD) is the most common type of senile dementia, which often develops in elderly or presenile individuals. As one of the pathological features of AD, amyloid β-protein (Aβ) causes energy dysmetabolism, thereby inducing cellular damage and apoptosis. Salidroside is the main active component of the traditional Chinese medicine Rhodiola. Previous studies have demonstrated that salidroside exerts a regulatory role in energy metabolism. However, the role and the mechanism of action of salidroside in AD remain unclear. Therefore, the present study used Aβ1–40 to induce damage in PC12 cells, thereby establishing a cell model of AD. In addition, salidroside treatment was performed to investigate the protective effect of salidroside and the underlying mechanisms. Aβ1-40-induced neuronal toxicity reduced cell viability and caused cellular damage. As a result, the expression level of nicotinamide phosphoribosyltransferase (NAMPT) decreased, the synthesis of nicotinamide adenine dinucleotide (NAD+; an energy metabolism-associated coenzyme) became insufficient, and the NAD+/nicotinamide adenine dinucleotide hydride ratio was reduced. Administration of salidroside alleviated Aβ-induced cell damage and increased the expression level of the key protein NAMPT and the synthesis of NAD+. The results of the present study demonstrate that salidroside exerts a protective effect on Aβ1-40-damaged PC12 cells. The underlying mechanism may be associated with the regulation of energy metabolism that relies predominantly on the NAMPT signaling pathway.
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