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苦参碱型瞬时受体电位 7 通道参与人参皂苷 Rd 诱导胃癌和乳腺癌细胞凋亡。

Involvement of melastatin type transient receptor potential 7 channels in ginsenoside Rd-induced apoptosis in gastric and breast cancer cells.

机构信息

Division of Longevity and Biofunctional Medicine, School of Korean Medicine, Pusan National University, Yangsan 626-870, Korea.

出版信息

J Ginseng Res. 2013 Apr;37(2):201-9. doi: 10.5142/jgr.2013.37.201.

DOI:10.5142/jgr.2013.37.201
PMID:23717173
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3659640/
Abstract

Ginsenoside, one of the active ingredients of Panax ginseng, has a variety of physiologic and pharmacologic effects. The purpose of this study was to explore the effects of ginsenoside Rd (G-Rd) on melastatin type transient receptor potential 7 (TRPM7) channels with respect to the proliferation and survival of AGS and MCF-7 cells (a gastric and a breast cancer cell line, respectively). AGS and MCF-7 cells were treated with different concentrations of G-Rd, and caspase-3 activities, mitochondrial depolarizations, and sub-G1 fractions were analyzed to determine if cell death occurred by apoptosis. In addition, human embryonic kidney (HEK) 293 cells overexpressing TRPM7 channels were used to confirm the role of TRPM7 channels. G-Rd inhibited the proliferation and survival of AGS and MCF-7 cells and enhanced caspase-3 activity, mitochondrial depolarization, and sub-G1 populations. In addition, G-Rd inhibited TRPM7-like currents in AGS and MCF-7 cells and in TRPM7 channel overexpressing HEK 293 cells, as determined by whole cell voltage-clamp recordings. Furthermore, TRPM7 overexpression in HEK 293 cells promoted G-Rd induced cell death. These findings suggest that G-Rd inhibits the proliferation and survival of gastric and breast cancer cells by inhibiting TRPM7 channel activity.

摘要

人参皂苷是人参的一种有效成分,具有多种生理和药理作用。本研究旨在探讨人参皂苷 Rd(G-Rd)对人胃癌细胞株 AGS 和人乳腺癌细胞株 MCF-7 增殖和存活的影响,及其对 melastatin 型瞬时受体电位 7(TRPM7)通道的作用。用不同浓度的 G-Rd 处理 AGS 和 MCF-7 细胞,分析 caspase-3 活性、线粒体去极化和亚 G1 区分数,以确定细胞死亡是否通过细胞凋亡发生。此外,还使用过表达 TRPM7 通道的人胚肾(HEK)293 细胞来确认 TRPM7 通道的作用。G-Rd 抑制 AGS 和 MCF-7 细胞的增殖和存活,并增强 caspase-3 活性、线粒体去极化和亚 G1 区分数。此外,通过全细胞膜片钳记录确定 G-Rd 抑制 AGS 和 MCF-7 细胞以及过表达 TRPM7 通道的 HEK 293 细胞中的 TRPM7 样电流。此外,HEK 293 细胞中 TRPM7 的过表达促进了 G-Rd 诱导的细胞死亡。这些发现表明,G-Rd 通过抑制 TRPM7 通道活性抑制胃癌和乳腺癌细胞的增殖和存活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/053a/3659640/4f8625ca5880/grosbr-37-201-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/053a/3659640/eb4c72009f88/grosbr-37-201-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/053a/3659640/5fd1a28cd237/grosbr-37-201-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/053a/3659640/64d3731d3dd9/grosbr-37-201-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/053a/3659640/6d7bc6d79ea5/grosbr-37-201-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/053a/3659640/4f8625ca5880/grosbr-37-201-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/053a/3659640/eb4c72009f88/grosbr-37-201-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/053a/3659640/5fd1a28cd237/grosbr-37-201-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/053a/3659640/64d3731d3dd9/grosbr-37-201-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/053a/3659640/6d7bc6d79ea5/grosbr-37-201-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/053a/3659640/4f8625ca5880/grosbr-37-201-g005.jpg

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Biotransformation of Ginsenoside Rb1 to Prosapogenins, Gypenoside XVII, Ginsenoside Rd, Ginsenoside F2, and Compound K by Leuconostoc mesenteroides DC102.肠膜明串珠菌 DC102 对人参皂苷 Rb1 向原人参二醇型皂苷、绞股蓝皂苷 XVII、人参皂苷 Rd、人参皂苷 F2 和化合物 K 的生物转化。
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