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假泽兰:对人肝癌(HepG2)细胞系的细胞毒性、细胞周期阻滞及氧化性DNA损伤

Verbesina encelioides: cytotoxicity, cell cycle arrest, and oxidative DNA damage in human liver cancer (HepG2) cell line.

作者信息

Al-Oqail Mai M, Siddiqui Maqsood A, Al-Sheddi Ebtesam S, Saquib Quaiser, Musarrat Javed, Al-Khedhairy Abdulaziz A, Farshori Nida N

机构信息

Department of Pharmacognosy, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.

Zoology Department, College of Science, King Saud University, P.O. Box-2455, Riyadh, 11451, Kingdom of Saudi Arabia.

出版信息

BMC Complement Altern Med. 2016 May 10;16:126. doi: 10.1186/s12906-016-1106-0.

DOI:10.1186/s12906-016-1106-0
PMID:27161012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4862229/
Abstract

BACKGROUND

Cancer is a major health problem and exploiting natural products have been one of the most successful methods to combat this disease. Verbesina encelioides is a notorious weed with various pharmacological properties. The aim of the present investigation was to screen the anticancer potential of V. encelioides extract against human lung cancer (A-549), breast cancer (MCF-7), and liver cancer (HepG2) cell lines.

METHODS

A-549, MCF-7, and HepG2 cells were exposed to various concentrations of (10-1000 μg/ml) of V. encelioides for 24 h. Further, cytotoxic concentrations (250, 500, and 1000 μg/ml) of V. encelioides induced oxidative stress (GSH and LPO), reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP), cell cycle arrest, and DNA damage in HepG2 cells were studied.

RESULTS

The exposure of cells to 10-1000 μg/ml of extract for 24 h, revealed the concentrations 250-1000 μg/ml was cytotoxic against MCF-7 and HepG2 cells, but not against A-549 cells. Moreover, the extract showed higher decrease in the cell viability against HepG2 cells than MCF-7 cells. Therefore, HepG2 cells were selected for further studies viz. oxidative stress (GSH and LPO), reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP), cell cycle arrest, and DNA damage. The results revealed differential anticancer activity of V. encelioides against A-549, MCF-7 and HepG2 cells. A significant induction of oxidative stress, ROS generation, and MMP levels was observed in HepG2 cells. The cell cycle analysis and comet assay showed that V. encelioides significantly induced G2/M arrests and DNA damage.

CONCLUSION

These results indicate that V. encelioides possess substantial cytotoxic potential and may warrant further investigation to develop potential anticancer agent.

摘要

背景

癌症是一个重大的健康问题,利用天然产物一直是对抗这种疾病最成功的方法之一。牛膝菊是一种具有多种药理特性的臭名昭著的杂草。本研究的目的是筛选牛膝菊提取物对人肺癌(A - 549)、乳腺癌(MCF - 7)和肝癌(HepG2)细胞系的抗癌潜力。

方法

将A - 549、MCF - 7和HepG2细胞暴露于不同浓度(10 - 1000μg/ml)的牛膝菊提取物中24小时。此外,研究了牛膝菊的细胞毒性浓度(250、500和1000μg/ml)对HepG2细胞诱导的氧化应激(谷胱甘肽和脂质过氧化)、活性氧(ROS)生成、线粒体膜电位(MMP)、细胞周期阻滞和DNA损伤。

结果

细胞暴露于10 - 1000μg/ml提取物24小时后,发现250 - 1000μg/ml的浓度对MCF - 7和HepG2细胞具有细胞毒性,但对A - 549细胞无细胞毒性。此外,提取物对HepG2细胞的细胞活力降低程度高于MCF - 7细胞。因此,选择HepG2细胞进行进一步研究,即氧化应激(谷胱甘肽和脂质过氧化)、活性氧(ROS)生成、线粒体膜电位(MMP)、细胞周期阻滞和DNA损伤。结果显示牛膝菊对A - 549、MCF - 7和HepG2细胞具有不同的抗癌活性。在HepG2细胞中观察到氧化应激、ROS生成和MMP水平的显著诱导。细胞周期分析和彗星试验表明,牛膝菊显著诱导G2/M期阻滞和DNA损伤。

结论

这些结果表明牛膝菊具有相当大的细胞毒性潜力,可能值得进一步研究以开发潜在的抗癌药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/30c0ef9b1a22/12906_2016_1106_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/75b737910f59/12906_2016_1106_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/158ed2314fe5/12906_2016_1106_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/553ad4735d9d/12906_2016_1106_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/2b120e7a7fff/12906_2016_1106_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/5c96a6e7d28f/12906_2016_1106_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/30c0ef9b1a22/12906_2016_1106_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/75b737910f59/12906_2016_1106_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/158ed2314fe5/12906_2016_1106_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/553ad4735d9d/12906_2016_1106_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/2b120e7a7fff/12906_2016_1106_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/5c96a6e7d28f/12906_2016_1106_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd7/4862229/30c0ef9b1a22/12906_2016_1106_Fig6_HTML.jpg

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