Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul, Republic of Korea.
Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul, Republic of Korea,
Pharmacology. 2020;105(9-10):586-597. doi: 10.1159/000505592. Epub 2020 Feb 4.
The accumulation of amyloid-β (Aβ) plaque in the brain is a characteristic feature of Alzheimer's disease (AD) and the cause of fatal oxidative damage to neuronal cells. Korean red ginseng (RG) is used extensively in traditional medicine and is known to have anti-oxidative and anti-inflammatory properties.
This study aims to investigate whether Korean RG extract inhibits Aβ-induced neuronal apoptosis.
Human neuronal cells (SH-SY5Y cells) were stimulated with Aβ (5 μmol/L) and treated with RG dissolved in phosphate-buffered saline (0.2, 2, 20 μg/mL).
RG suppressed the reduction of cell viability and the increase in apoptotic factors (Bax/Bcl-2 ratio and caspase-3 activity) in Aβ-treated cells. RG suppressed Aβ-induced increases in intracellular and mitochondrial reactive oxygen species (ROS) levels and mitochondrial dysfunction (determined by low mitochondrial membrane potential and oxygen consumption rate) in a dose-dependent manner. RG inhibited nuclear factor kappa-light-chain-enhancer of activated B cells (NF-ĸB) activation and expression of the pro-apoptotic gene Nucling in Aβ-treated cells.
RG confers protection against neuronal apoptosis by reducing ROS levels and suppressing mitochondrial dysfunction and NF-κB activation, which results in suppression of NF-κB-mediated activation of Nucling expression in Aβ-treated cells. Supplementation with RG may be beneficial for preventing Aβ-induced neuronal cell death associated with AD.
脑内淀粉样β（Aβ）斑块的积累是阿尔茨海默病（AD）的一个特征，也是导致神经元细胞致命氧化损伤的原因。韩国红参（RG）在传统医学中被广泛应用，具有抗氧化和抗炎特性。
本研究旨在探讨韩国 RG 提取物是否抑制 Aβ诱导的神经元细胞凋亡。
用人神经母细胞瘤细胞（SH-SY5Y 细胞）用 Aβ（5 μmol/L）刺激，并以溶解在磷酸盐缓冲液中的 RG（0.2、2、20 μg/mL）进行处理。
RG 抑制了 Aβ处理细胞中细胞活力降低和凋亡因子（Bax/Bcl-2 比值和 caspase-3 活性）增加。RG 以剂量依赖的方式抑制 Aβ诱导的细胞内和线粒体活性氧（ROS）水平增加和线粒体功能障碍（由低线粒体膜电位和耗氧量决定）。RG 抑制了 Aβ处理细胞中核因子 kappa-轻链增强子的 B 细胞（NF-κB）激活和促凋亡基因 Nucling 的表达。
RG 通过降低 ROS 水平、抑制线粒体功能障碍和 NF-κB 激活来对神经元细胞凋亡提供保护，从而抑制 Aβ 处理细胞中 NF-κB 介导的 Nucling 表达激活。RG 的补充可能有益于预防 AD 相关的 Aβ 诱导的神经元细胞死亡。
