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水提物诱导人肝癌细胞凋亡。

Aqueous extract induces cell apoptosis in human hepatocellular carcinoma cells.

机构信息

Institute of Molecular Biology College of Life Science, National Chung Hsing University, Taichung, Taiwan.

Division of Chest Medicine, Department of Internal Medicine, Taichung Hospital, Ministry of Health and Welfare, Taichung, Taiwan.

出版信息

Int J Med Sci. 2020 Jan 18;17(3):338-346. doi: 10.7150/ijms.39436. eCollection 2020.

DOI:10.7150/ijms.39436
PMID:32132869
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7053345/
Abstract

Treatment of advanced hepatocellular carcinoma (HCC) has exhibited a poor overall survival rate of only six to ten months, and the urgency of the development of more effective novel agents is ever present. In this line of research, we aimed to investigate the effects and inhibitive mechanisms of aqueous leaf extract (OGE), the extract of , which is commonly used as a therapeutic herb for its numerous pharmacological properties, on malignant HCC cells. Our results showed that OGE decreased the cell viability of HCC SK-Hep1 and HA22T cells in a dose-dependent manner (from 400 to 800 µg/mL), while there is little effect on Chang liver cells. Moreover, cell-cycle analysis shows increased Sub-G1 cell count in SK-Hep1 and HA22T cells which is not observed in Chang liver cells. These findings raise suspicion that the OGE-induced cell death may be mediated through proteins that regulate cell cycle and apoptosis in SK-Hep1 and HA22T cells, and further experimentation revealed that OGE treatment resulted in a dose-dependent decrease in caspase 3 and PARP expressions and in CDK4and p-ERK1/2expressions. Moreover, animal tests also exhibited decreased HCC tumor growth by OGE treatment. We therefore suggest that the inhibition of cell viability and tumor growth induced by OGE may be correlated to the alteration of apoptosis-related proteins.

摘要

治疗晚期肝细胞癌 (HCC) 的总体存活率仅为 6 至 10 个月,因此迫切需要开发更有效的新型药物。在这一研究领域中,我们旨在研究水提叶提取物(OGE)对恶性 HCC 细胞的作用及其抑制机制。该提取物来自 ,常被用作治疗多种疾病的草药,具有多种药理学特性。我们的研究结果表明,OGE 以剂量依赖的方式降低 HCC SK-Hep1 和 HA22T 细胞的活力(400 至 800µg/mL),而对 Chang 肝细胞几乎没有影响。此外,细胞周期分析显示 SK-Hep1 和 HA22T 细胞中 Sub-G1 细胞计数增加,而 Chang 肝细胞中未观察到这种情况。这些发现表明,OGE 诱导的细胞死亡可能是通过调节 SK-Hep1 和 HA22T 细胞细胞周期和凋亡的蛋白质介导的,进一步的实验表明,OGE 处理导致 caspase 3 和 PARP 表达以及 CDK4 和 p-ERK1/2 表达呈剂量依赖性下降。此外,动物试验也显示 OGE 处理可降低 HCC 肿瘤生长。因此,我们认为 OGE 诱导的细胞活力和肿瘤生长抑制可能与凋亡相关蛋白的改变有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87ab/7053345/07eff7b498f4/ijmsv17p0338g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87ab/7053345/34250e21633c/ijmsv17p0338g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87ab/7053345/acc8a9ea7d3f/ijmsv17p0338g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87ab/7053345/07eff7b498f4/ijmsv17p0338g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87ab/7053345/34250e21633c/ijmsv17p0338g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87ab/7053345/b63356b7eb65/ijmsv17p0338g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87ab/7053345/70fb3bdc80c7/ijmsv17p0338g003.jpg
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