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乙醇提取物在异种移植白血病模型中的抗癌疗效

Anticancer Efficacy of Ethanol Extract in a Xenografted Leukemia Model.

作者信息

Park Jae Gwang, Son Young-Jin, Lee Tae Ho, Baek Nam Joon, Yoon Deok Hyo, Kim Tae Woong, Aravinthan Adithan, Hong Sungyoul, Kim Jong-Hoon, Sung Gi-Ho, Cho Jae Youl

机构信息

Department of Genetic Engineering, Sungkyunkwan University, Suwon 16419, Republic of Korea.

Department of Pharmacy, Sunchon National University, Suncheon 57922, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2017;2017:8474703. doi: 10.1155/2017/8474703. Epub 2017 Jul 6.

DOI:10.1155/2017/8474703
PMID:28761499
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5518515/
Abstract

is used widely as a traditional medicine in East Asia. Although a few studies have attempted to elucidate the anticancer activities of , the precise mechanism of therapeutic effects is not fully understood. We examined the anticancer activities of ethanolic extract (Cm-EE) and its cellular and molecular mechanisms. For this purpose, a xenograft mouse model bearing murine T cell lymphoma (RMA) cell-derived cancers was established to investigate in vivo anticancer mechanisms. MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay, immunoblotting analysis, and flow cytometric assay were employed to check in vitro cytotoxicity, molecular targets, and proapoptotic action of Cm-EE. Interestingly, cancer sizes and mass were reduced in a -administered group. Levels of the phosphorylated forms of p85 and AKT were clearly decreased in the group administered with Cm-EE. This result indicated that levels of phosphoglycogen synthase kinase 3 (p-GSK3) and cleaved caspase-3 were increased with orally administered Cm-EE. In addition, Cm-EE directly inhibited the viability of cultured RMA cells and C6 glioma cells. The number of proapoptotic cells was significantly increased in a Cm-EE treated group compared with a control group. Our results suggested that might be able to inhibit cancer growth through regulation of p85/AKT-dependent or GSK3-related caspase-3-dependent apoptosis.

摘要

在东亚地区被广泛用作传统药物。尽管有一些研究试图阐明其抗癌活性,但其治疗效果的确切机制尚未完全了解。我们研究了[具体药物名称]乙醇提取物(Cm-EE)的抗癌活性及其细胞和分子机制。为此,建立了携带鼠T细胞淋巴瘤(RMA)细胞衍生癌症的异种移植小鼠模型,以研究体内抗癌机制。采用MTT [3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐] 法、免疫印迹分析和流式细胞术检测Cm-EE的体外细胞毒性、分子靶点和促凋亡作用。有趣的是,在给予[具体药物名称]的组中,肿瘤大小和质量减小。在给予Cm-EE的组中,p85和AKT的磷酸化形式水平明显降低。该结果表明,口服Cm-EE可使磷酸糖原合酶激酶3(p-GSK3)和裂解的半胱天冬酶-3水平升高。此外,Cm-EE直接抑制培养的RMA细胞和C6胶质瘤细胞的活力。与对照组相比,Cm-EE处理组中促凋亡细胞的数量显著增加。我们的结果表明,[具体药物名称]可能能够通过调节p85/AKT依赖性或GSK3相关的半胱天冬酶-3依赖性凋亡来抑制癌症生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1e/5518515/ab7fec2a28af/ECAM2017-8474703.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1e/5518515/fd6020261d6a/ECAM2017-8474703.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1e/5518515/6b7dde056bf8/ECAM2017-8474703.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1e/5518515/5ac9c6b130d9/ECAM2017-8474703.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1e/5518515/ab7fec2a28af/ECAM2017-8474703.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1e/5518515/fd6020261d6a/ECAM2017-8474703.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1e/5518515/6b7dde056bf8/ECAM2017-8474703.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1e/5518515/5ac9c6b130d9/ECAM2017-8474703.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1e/5518515/ab7fec2a28af/ECAM2017-8474703.004.jpg

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