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人参皂苷化合物 K 可诱导年轻和老年小鼠海马区的成年神经前体细胞增殖和新生细胞存活。

Ginsenoside Compound K Induces Adult Hippocampal Proliferation and Survival of Newly Generated Cells in Young and Elderly Mice.

机构信息

Department of Physiology, Chonbuk National University Medical School, Jeonju-si, Jeollabuk-do 54907, Korea.

Brain Korea 21 Plus Program, Chonbuk National University Medical School, Jeonju-si 54907, Korea.

出版信息

Biomolecules. 2020 Mar 23;10(3):484. doi: 10.3390/biom10030484.

DOI:10.3390/biom10030484
PMID:32210026
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7175218/
Abstract

Cognitive impairment can be associated with reduced adult hippocampal neurogenesis, and it may contribute to age-associated neurodegenerative diseases such as Alzheimer's (AD). Compound K (CK) is produced from the protopanaxadiol (PPD)-type ginsenosides Rb1, Rb2, and Rc by intestinal microbial conversion. Although CK has been reported as an inducing effector for neuroprotection and improved cognition in hippocampus, its effect on adult neurogenesis has not been explored yet. Here, we investigated the effect of CK on hippocampal neurogenesis in both young (2 months) and elderly (24 months) mice. CK treatment increased the number of cells co-labeled with 5-ethynyl-2'-deoxyuridine (EdU) and proliferating cell nuclear antigen (PCNA); also, Ki67, specific markers for progenitor cells, was more expressed, thus enhancing the generation of new cells and progenitor cells in the dentate gyrus of both young and elderly mice. Moreover, CK treatment increased the number of cells co-labeled with EdU and NeuN, a specific marker for mature neuron in the dentate gyrus, suggesting that newly generated cells survived and differentiated into mature neurons at both ages. These findings demonstrate that CK increases adult hippocampal neurogenesis, which may be beneficial against neurodegenerative disorders such as AD.

摘要

认知障碍与成人海马神经发生减少有关,它可能导致与年龄相关的神经退行性疾病,如阿尔茨海默病(AD)。化合物 K(CK)是由肠道微生物转化原人参二醇(PPD)型人参皂苷 Rb1、Rb2 和 Rc 产生的。尽管 CK 已被报道为一种诱导神经保护和改善海马认知的效应物,但它对成年神经发生的影响尚未被探索。在这里,我们研究了 CK 对年轻(2 个月)和老年(24 个月)小鼠海马神经发生的影响。CK 处理增加了与 5-乙炔基-2'-脱氧尿苷(EdU)和增殖细胞核抗原(PCNA)共标记的细胞数量;此外,Ki67,祖细胞的特异性标志物,表达更多,从而增强了年轻和老年小鼠齿状回中新细胞和祖细胞的生成。此外,CK 处理增加了 EdU 和神经元核抗原(NeuN)共标记的细胞数量,NeuN 是齿状回中成熟神经元的特异性标志物,表明新生成的细胞存活并在两个年龄阶段分化为成熟神经元。这些发现表明 CK 增加了成年海马神经发生,这可能对 AD 等神经退行性疾病有益。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/327250665312/biomolecules-10-00484-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/688c55c9a91c/biomolecules-10-00484-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/ccee06738ff0/biomolecules-10-00484-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/bc34bd05b261/biomolecules-10-00484-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/e891868ec8a2/biomolecules-10-00484-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/439795470e04/biomolecules-10-00484-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/6a08cb7a349c/biomolecules-10-00484-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/327250665312/biomolecules-10-00484-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/688c55c9a91c/biomolecules-10-00484-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/ccee06738ff0/biomolecules-10-00484-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/bc34bd05b261/biomolecules-10-00484-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/e891868ec8a2/biomolecules-10-00484-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/439795470e04/biomolecules-10-00484-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/6a08cb7a349c/biomolecules-10-00484-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/7175218/327250665312/biomolecules-10-00484-g007.jpg

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