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姜黄素诱导人宫颈癌 HeLa 细胞氧化应激介导的细胞毒性、细胞周期停滞和凋亡。

Oxidative Stress Mediated Cytotoxicity, Cell Cycle Arrest, and Apoptosis Induced by in Human Cervical Cancer HeLa Cells.

机构信息

Department of Pharmacognosy, College of Pharmacy, King Saud University, Riyadh 11495, Saudi Arabia.

DNA Research Chair, Zoology Department, College of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia.

出版信息

Oxid Med Cell Longev. 2021 Jan 28;2021:6695634. doi: 10.1155/2021/6695634. eCollection 2021.

DOI:10.1155/2021/6695634
PMID:33574980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7861940/
Abstract

Mill (Damask rose), belonging to the Rosaceae family, is known for medicinal purposes in traditional medicine system. However, its anticancer activity has not been studied yet in detail. Herein, we aimed to investigate the cytotoxic effects of hexane (RA-HE) and methanolic (RA-ME) extracts against human breast (MCF-7), lung epithelial (A-549), and cervical (HeLa) cancer cells. The RA-HE and RA-ME showed more potent cytotoxic effects against HeLa cells with an IC of 819.6 and 198.4 g/ml, respectively. Further, cytotoxic concentrations of most effective extract (RA-ME) were used to evaluate the mechanism of cytotoxicity involved in HeLa cells. A concentration-dependent induction of lipid peroxidation (LPO) and reduction of glutathione (GSH) in HeLa cells treated with 250-1000 g/ml of RA-ME confirms the association of oxidative stress. We also detected a noteworthy increase in reactive oxygen species (ROS) production and a decline in mitochondrial membrane potential (MMP) level in RA-ME-exposed HeLa cells. Flow cytometric data showed a strong dose-response relationship in cell cycle analysis between subG1 phase in HeLa cells and RA-ME treatment. Similarly, a concentration-dependent increase was recorded with Annexin V assay in HeLa cells going to late apoptosis. In conclusion, our findings suggest that RA-ME-induced cytotoxicity and apoptosis in HeLa cells are mediated by oxidative stress.

摘要

玫瑰(大马士革玫瑰),属于蔷薇科,在传统医学体系中被用于药用目的。然而,其抗癌活性尚未得到详细研究。在此,我们旨在研究己烷(RA-HE)和甲醇(RA-ME)提取物对人乳腺癌(MCF-7)、肺上皮(A-549)和宫颈(HeLa)癌细胞的细胞毒性作用。RA-HE 和 RA-ME 对 HeLa 细胞表现出更强的细胞毒性作用,其 IC 分别为 819.6 和 198.4μg/ml。此外,用最有效的提取物(RA-ME)的细胞毒性浓度来评估其对 HeLa 细胞的细胞毒性机制。在浓度依赖性下,用 250-1000μg/ml 的 RA-ME 处理 HeLa 细胞,诱导脂质过氧化(LPO)和谷胱甘肽(GSH)减少,这证实了氧化应激的关联。我们还检测到 RA-ME 暴露的 HeLa 细胞中活性氧(ROS)产生显著增加和线粒体膜电位(MMP)水平下降。流式细胞术数据显示,在 HeLa 细胞的亚 G1 期和 RA-ME 处理之间的细胞周期分析中存在强烈的剂量反应关系。同样,在 Annexin V 测定中,在 HeLa 细胞中记录到浓度依赖性的晚期凋亡增加。总之,我们的研究结果表明,RA-ME 诱导的 HeLa 细胞的细胞毒性和凋亡是由氧化应激介导的。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d93/7861940/8cf534639909/OMCL2021-6695634.008.jpg

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