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人参皂苷化合物 K 通过激活 MEK/ERK1/2 和 PI3K/AKT 通路促进许旺细胞的增殖、迁移和分化。

Ginsenoside Compound K Promotes Proliferation, Migration and Differentiation of Schwann Cells via the Activation of MEK/ERK1/2 and PI3K/AKT Pathways.

机构信息

Department of Pharmacy, Yantai Affiliated Hospital of Binzhou Medical College, Mouping District, Yantai city, Shandong Province, China.

Special Examination Department of Yantai Affiliated Hospital of Binzhou Medical College, Muping District, Yantai, Shandong, China.

出版信息

Neurochem Res. 2021 Jun;46(6):1400-1409. doi: 10.1007/s11064-021-03279-0. Epub 2021 Mar 18.

DOI:10.1007/s11064-021-03279-0
PMID:33738663
Abstract

The proliferation and differentiation of Schwann cells are critical for the remyelination of injured peripheral nerve. Ginsenoside compound K (CK) is a metabolite produced from ginsenoside Rb1 which has strong anti-inflammatory effects. However, the potential effects of CK on Schwann cells have not been studied systematically before. Therefore, this study was aimed to explore the functions of CK in Schwann cell proliferation, migration and differentiation and its potential regulatory mechanism. Primary Schwann cells and RSC96 cells were treated with or without CK at different doses. The proliferation and migration of primary Schwann cells and RSC96 cells were examined by Cell Counting Kit-8 (CCK-8) and Transwell assays, respectively. The mRNA expression of myelin-associated glycoprotein (MAG) and myelin basic protein (MBP) was tested by quantitative real-time polymerase chain reaction (qRT-PCR). The levels of all proteins were examined by Western blot. CK could promote cell proliferation, migration and induce MAG and MBP expression in primary Schwann cells and RSC96 cells. Furthermore, CK activated MEK/ERK1/2 and PI3K/AKT pathways, and the beneficial effects of CK on primary Schwann cells and RSC96 cells were distinctly suppressed by inhibitor PD98059 or LY294002. Ginsenoside compound K induced cell proliferation, migration and differentiation via the activation of MEK/ERK1/2 and PI3K/AKT pathways in cultured primary Schwann cells and RSC96 cells.

摘要

雪旺细胞的增殖和分化对于损伤外周神经的髓鞘再生至关重要。人参皂苷化合物 K(CK)是从人参皂苷 Rb1 产生的一种代谢物,具有很强的抗炎作用。然而,CK 对雪旺细胞的潜在影响以前没有系统地研究过。因此,本研究旨在探讨 CK 对雪旺细胞增殖、迁移和分化的作用及其潜在的调节机制。用或不用不同剂量 CK 处理原代雪旺细胞和 RSC96 细胞。通过细胞计数试剂盒-8(CCK-8)和 Transwell 测定分别检测原代雪旺细胞和 RSC96 细胞的增殖和迁移。通过定量实时聚合酶链反应(qRT-PCR)检测髓鞘相关糖蛋白(MAG)和髓鞘碱性蛋白(MBP)的 mRNA 表达。通过 Western blot 检测所有蛋白的水平。CK 可促进原代雪旺细胞和 RSC96 细胞的增殖、迁移,并诱导 MAG 和 MBP 表达。此外,CK 激活了 MEK/ERK1/2 和 PI3K/AKT 通路,而 CK 对原代雪旺细胞和 RSC96 细胞的有益作用被 MEK/ERK1/2 和 PI3K/AKT 通路抑制剂 PD98059 或 LY294002 明显抑制。人参皂苷化合物 K 通过激活 MEK/ERK1/2 和 PI3K/AKT 通路诱导培养的原代雪旺细胞和 RSC96 细胞增殖、迁移和分化。

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人参皂苷Compound K通过抑制蛋白酪氨酸磷酸酶1B(PTP1B)介导的胰岛素受体底物1(IRS1)酪氨酸去磷酸化来减少缺血/再灌注诱导的神经元凋亡。
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