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来自[具体来源]的苯乙醇苷通过线粒体依赖性途径诱导细胞凋亡,从而抑制B16-F10细胞的生长。 (注:原文中“from”后缺少具体来源信息)

Phenylethanoid Glycosides from Inhibits the Growth of B16-F10 Cells both and by Induction of Apoptosis via Mitochondria-dependent Pathway.

作者信息

Li Jinyu, Li Jinyao, Aipire Adila, Gao Li, Huo Shixia, Luo Jiaojiao, Zhang Fuchun

机构信息

Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.

Xinjiang Laboratory of Uyghur Medical Prescription, Xinjiang Institute of Traditional Uyghur Medicine, Urumqi, Xinjiang, China.

出版信息

J Cancer. 2016 Sep 12;7(13):1877-1887. doi: 10.7150/jca.15512. eCollection 2016.

Abstract

phenylethanoid glycosides (CTPG) have been shown various biological activities including anti-allergy, hepatoprotective activity and bone regeneration. However, the anti-tumor activity of CTPG needs to be investigated. CTPG was used to treat B16-F10 cells both and . We found that CTPG dramatically changed the morphology of B16-F10 cells, and significantly reduced the viability of B16-F10 cells in a dose-dependent and time-dependent manner, which might be mediated by CTPG-induced apoptosis and cell cycle arrest. After CTPG treatment, the expressions of BAX and BCL-2 were up-regulated and down-regulated, respectively. Moreover, mitochondrial membrane potential was reduced and ROS generation was increased. Consequently, the levels of cytochrome c and cleaved-caspase-3 and -9 were up-regulated by CTPG treatment but not for cleaved-caspase-8. We further observed that CTPG significantly inhibited the tumor growth and improved the survival rate of tumor mice. We also observed that CTPG promoted the proliferation of splenocytes and increased the proportions of CD4 and CD8 T cells in spleens of tumor mice. The results showed that CTPG induced the apoptosis of B16-F10 cells through mitochondria-dependent pathway, suggesting that CTPG could be a potential candidate for treatment of cancer.

摘要

苯乙醇苷(CTPG)已显示出多种生物活性,包括抗过敏、肝脏保护活性和骨再生。然而,CTPG的抗肿瘤活性有待研究。CTPG用于处理B16 - F10细胞。我们发现CTPG显著改变了B16 - F10细胞的形态,并以剂量和时间依赖性方式显著降低了B16 - F10细胞的活力,这可能是由CTPG诱导的细胞凋亡和细胞周期停滞介导的。CTPG处理后,BAX和BCL - 2的表达分别上调和下调。此外,线粒体膜电位降低,活性氧生成增加。因此,CTPG处理上调了细胞色素c以及裂解的半胱天冬酶 - 3和 - 9的水平,但未上调裂解的半胱天冬酶 - 8的水平。我们进一步观察到CTPG显著抑制肿瘤生长并提高了荷瘤小鼠的存活率。我们还观察到CTPG促进了脾细胞的增殖,并增加了荷瘤小鼠脾脏中CD4和CD8 T细胞的比例。结果表明,CTPG通过线粒体依赖性途径诱导B16 - F10细胞凋亡,提示CTPG可能是一种潜在的癌症治疗候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b5d/5039372/4b0b0dedc1fb/jcav07p1877g001.jpg

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