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氧化应激在 63T 诱导的人肺癌和正常肺成纤维细胞系细胞毒性中的作用。

The role of oxidative stress in 63 T-induced cytotoxicity against human lung cancer and normal lung fibroblast cell lines.

机构信息

Department of Toxicology, Poznan University of Medical Sciences, Dojazd 30 Street, 60-631, Poznan, Poland.

Department of Immunology, Poznan University of Medical Sciences, Poznan, Poland.

出版信息

Invest New Drugs. 2019 Oct;37(5):849-864. doi: 10.1007/s10637-018-0704-8. Epub 2018 Nov 29.

Abstract

It has been shown previously that molecules built on benzanilide and thiobenzanilide scaffolds possess differential biological properties including selective anticancer activity. In our previous study, we examined the cytotoxic activity and mechanism of action of the thiobenzanilide derivative N,N'-(1,2-phenylene)bis3,4,5-trifluorobenzothioamide (63 T) as a potential chemotherapeutic compound in an experimental model employing A549 lung adenocarcinoma cells and CCD39Lu non-tumorigenic lung fibroblasts. Since the results suggested oxidative stress as a co-existing mechanism of the cytotoxic effect exerted by 63 T on tested cells, studies involving the analysis of reactive oxygen species (ROS) generation and markers of oxidative stress in cells incubated with 63 T were carried out. It may be concluded that the selective activity of 63 T against cancer cells shown in our experiments is caused, at least in part, by the response of the tested cells to 63 T mediated oxidative stress in both tested cell lines.

摘要

先前的研究表明,以苯甲酰苯胺和硫代苯甲酰苯胺为骨架构建的分子具有不同的生物学特性,包括选择性抗癌活性。在我们之前的研究中,我们研究了噻吩并苯甲酰苯胺衍生物 N,N'-(1,2-亚苯基)双-3,4,5-三氟苯硫酰胺 (63T) 的细胞毒性活性和作用机制,作为一种潜在的化疗化合物,在实验模型中使用 A549 肺腺癌细胞和 CCD39Lu 非致瘤性肺成纤维细胞。由于结果表明氧化应激是 63T 对测试细胞产生细胞毒性作用的共存机制之一,因此进行了涉及分析与 63T 孵育的细胞中活性氧 (ROS) 生成和氧化应激标志物的研究。可以得出结论,我们实验中 63T 对癌细胞的选择性活性至少部分是由测试细胞对两种测试细胞系中 63T 介导的氧化应激的反应引起的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0aff/6736908/dd9e6a8d8a51/10637_2018_704_Fig1_HTML.jpg

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