Shin Soo Jung, Park Yong Ho, Jeon Seong Gak, Kim Sujin, Nam Yunkwon, Oh Sang-Muk, Lee Yong Yook, Moon Minho
Department of Biochemistry, College of Medicine, Konyang University, Daejeon 35365, Republic of Korea.
The Korean Ginseng Research Institute, Korea Ginseng Corporation, Gajeong-ro 30, Shinseong-dong, Yuseong-gu, Daejeon 34128, Republic of Korea.
Oxid Med Cell Longev. 2020 Jun 30;2020:7829842. doi: 10.1155/2020/7829842. eCollection 2020.
Tau, a microtubule-associated protein expressed in mature neurons, interacts with tubulin to promote the assembly and stabilization of microtubules. However, abnormally hyperphosphorylated tau dissociates from microtubules and self-aggregates. Tau aggregates, including paired helical filaments and neurofibrillary tangles, promote neuronal dysfunction and death and are the defining neuropathological feature of tauopathies. Therefore, suppressing tau aggregation or stimulating the dissociation of tau aggregates has been proposed as an effective strategy for treating neurodegenerative diseases associated with tau pathology such as Alzheimer's disease (AD) and frontotemporal dementia. Interestingly, ginsenosides extracted from reduced the hippocampal and cortical expression of phosphorylated tau in a rat model of AD. However, no studies have been conducted into the effect of red ginseng (RG) and its components on tau pathology. Here, we evaluated the effect of Korean red ginseng extract (KRGE) and its components on the aggregation and disassociation of tau. Using the thioflavin T assay, we monitored the change in fluorescence produced by the aggregation or disassociation of tau K18, an aggregation-prone fragment of tau containing the microtubule-binding domain. Our analysis revealed that KRGE not only inhibited tau aggregation but also promoted the dissociation of tau aggregates. In addition, the KRGE fractions, such as saponin, nonsaponin, and nonsaponin fraction with rich polysaccharide, also inhibited tau aggregation and promoted the dissociation of tau aggregates. Our observations suggest that RG could be a potential therapeutic agent for the treatment of neurodegenerative diseases associated with tauopathy.
Tau是一种在成熟神经元中表达的微管相关蛋白，它与微管蛋白相互作用以促进微管的组装和稳定。然而，异常过度磷酸化的tau会从微管上解离并自我聚集。Tau聚集体，包括双螺旋丝和神经原纤维缠结，会促进神经元功能障碍和死亡，并且是tau蛋白病的决定性神经病理学特征。因此，抑制tau聚集或刺激tau聚集体的解离已被提议作为治疗与tau病理学相关的神经退行性疾病（如阿尔茨海默病（AD）和额颞叶痴呆）的有效策略。有趣的是，从[具体来源未提及]中提取的人参皂苷降低了AD大鼠模型中磷酸化tau在海马体和皮质中的表达。然而，尚未有关于红参（RG）及其成分对tau病理学影响的研究。在此，我们评估了韩国红参提取物（KRGE）及其成分对tau聚集和解离的影响。使用硫黄素T测定法，我们监测了tau K18（tau的一个易聚集片段，包含微管结合结构域）聚集或解离所产生的荧光变化。我们的分析表明，KRGE不仅抑制tau聚集，还促进tau聚集体的解离。此外，KRGE组分，如皂苷、非皂苷以及富含多糖的非皂苷组分，也抑制tau聚集并促进tau聚集体的解离。我们的观察结果表明，RG可能是治疗与tau蛋白病相关的神经退行性疾病的潜在治疗剂。
