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人参炔三醇增强少突胶质细胞系细胞的增殖、晚期分化以及内质网应激后的细胞存活能力。

Gintonin Enhances Proliferation, Late Stage Differentiation, and Cell Survival From Endoplasmic Reticulum Stress of Oligodendrocyte Lineage Cells.

作者信息

Mijan Mohammad Al, Kim Ji Young, Moon So-Young, Choi Sun-Hye, Nah Seung-Yeol, Yang Hyun-Jeong

机构信息

Department of Integrative Biosciences, University of Brain Education, Cheonan, South Korea.

Korea Institute of Brain Science, Seoul, South Korea.

出版信息

Front Pharmacol. 2019 Oct 8;10:1211. doi: 10.3389/fphar.2019.01211. eCollection 2019.

DOI:10.3389/fphar.2019.01211
PMID:31680979
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6797839/
Abstract

Although evidence on myelin diseases is steadily accumulating, effective preventive or therapeutic strategies against them have not been established so far. Ginseng is well known for its beneficial effects on health and diseases; however, detailed studies on ginseng's effects on myelin-producing oligodendrocytes have not been performed yet. In this study, we investigated the function of gintonin-an active component of ginseng-on the proliferation, differentiation, and survival of oligodendrocyte lineage cells. We performed real-time percutaneous coronary intervention, Western blot, and immunocytochemistry on primary oligodendrocyte precursor cell cultures and myelinating co-cultures. Our results show that gintonin stimulates oligodendrocyte precursor cell proliferation. Gintonin's effect was inhibited by Ki16425, an antagonist of lysophosphatidic acid 1/3 receptors. Interestingly, with regard to cell differentiation, gintonin facilitated late differentiation of oligodendrocyte development, but not early differentiation. Moreover, it showed protective effects on oligodendrocyte lineage cells against endoplasmic reticulum stress-induced cell death, potentially by modulating unfolded protein responses. Our results suggest that gintonin is a potential therapeutic candidate in the treatment of myelin diseases.

摘要

尽管关于髓鞘疾病的证据在不断积累,但迄今为止尚未建立有效的预防或治疗策略。人参因其对健康和疾病的有益作用而闻名;然而,尚未对人参对产生髓鞘的少突胶质细胞的作用进行详细研究。在本研究中,我们研究了人参的活性成分人参皂苷对少突胶质细胞系细胞的增殖、分化和存活的作用。我们对原代少突胶质前体细胞培养物和髓鞘形成共培养物进行了实时经皮冠状动脉介入、蛋白质印迹和免疫细胞化学分析。我们的结果表明,人参皂苷刺激少突胶质前体细胞增殖。人参皂苷的作用被溶血磷脂酸1/3受体拮抗剂Ki16425抑制。有趣的是,在细胞分化方面,人参皂苷促进少突胶质细胞发育的晚期分化,但不促进早期分化。此外,它对少突胶质细胞系细胞具有保护作用,可抵抗内质网应激诱导的细胞死亡,可能是通过调节未折叠蛋白反应来实现的。我们的结果表明,人参皂苷是治疗髓鞘疾病的潜在治疗候选物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/b3cee1497f20/fphar-10-01211-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/5af7f9ecaf2c/fphar-10-01211-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/83049a1ab870/fphar-10-01211-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/87c649a50674/fphar-10-01211-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/dae0bbd97d6c/fphar-10-01211-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/b3cee1497f20/fphar-10-01211-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/5af7f9ecaf2c/fphar-10-01211-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/567efca2540a/fphar-10-01211-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/83049a1ab870/fphar-10-01211-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/87c649a50674/fphar-10-01211-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/dae0bbd97d6c/fphar-10-01211-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c7/6797839/b3cee1497f20/fphar-10-01211-g006.jpg

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