Department of Food Science and Nutrition, Dong-A University, 37, Nakdong-daero 550 beon-gil, Saha-gu, Busan 49315, Korea.
Department of Food & Life Science, College of Biomedical Science & Engineering, Inje University, 197, Inje-ro, Gimhae-si, Gyeongsangnam-do 50834, Korea.
Int J Mol Sci. 2017 Oct 23;18(10):2218. doi: 10.3390/ijms18102218.
One of pathological characteristics of Alzheimer's disease (AD), aggregation and deposition of β amyloid (Aβ), has been accepted as a potent activator of neuronal cell death. Red ginseng is well-known for various pharmacological activities, but most studies have been focused on red ginseng water extract (RGW), which has resulted in the conception of the present study of red ginseng oil (RGO) against Aβ-induced neurotoxicity. Cytotoxicity and apoptosis induction by Aβ were verified and the underlying mechanism by which RGO inhibited neuronal cell death, mitochondria dysfunction and NF-κB pathway related protein markers were evaluated. RGO attenuated Aβ-induced apoptosis, not only by inhibiting calcium influx, but also by reducing mitochondrial membrane potential loss. RGO significantly decreased Bax, whereas increased Bcl-2 and inactivated of caspase-3 and -9 and PARP-1 stimulated by Aβ. Anti-neuroinflammatory effect of RGO was demonstrated by downregulating c-Jun N-terminal kinase (JNK) and p38, resulting in inhibiting of the NF-κB pathway and thereby suppressing the expressions of pro-inflammatory mediators such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E₂ (PGE₂), nitric oxide (NO) and tumor necrosis factor-α (TNF-α). The present study revealed that RGO is a potential natural resource of the functional foods industry as well as a promising candidate of multi-target neuronal protective agent for the prevention of AD.
阿尔茨海默病（AD）的病理特征之一是β淀粉样蛋白（Aβ）的聚集和沉积，它被认为是神经元细胞死亡的有效激活剂。红参以多种药理活性而闻名，但大多数研究都集中在红参水提取物（RGW）上，这导致了本研究对红参油（RGO）对抗 Aβ诱导的神经毒性的研究。验证了 Aβ诱导的细胞毒性和细胞凋亡，并评估了 RGO 抑制神经元细胞死亡、线粒体功能障碍和 NF-κB 途径相关蛋白标志物的潜在机制。RGO 不仅通过抑制钙内流，而且通过减少线粒体膜电位丧失来减轻 Aβ诱导的细胞凋亡。RGO 显著降低 Bax，同时增加 Bcl-2 并失活 Aβ 刺激的 caspase-3 和 -9 及 PARP-1。RGO 的抗神经炎症作用通过下调 c-Jun N 末端激酶（JNK）和 p38 来证明，从而抑制 NF-κB 途径，从而抑制诱导型一氧化氮合酶（iNOS）、环氧化酶-2（COX-2）、前列腺素 E₂（PGE₂）、一氧化氮（NO）和肿瘤坏死因子-α（TNF-α）等促炎介质的表达。本研究表明，RGO 是功能性食品工业的潜在天然资源，也是预防 AD 的多靶点神经保护剂的有前途的候选药物。
