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干杏多酚通过线粒体依赖途径诱导细胞凋亡抑制A549人肺腺癌细胞生长。

Dried Apricot Polyphenols Suppress the Growth of A549 Human Lung Adenocarcinoma Cells by Inducing Apoptosis via a Mitochondrial-Dependent Pathway.

作者信息

Zhao Caiyun, Wang Jingteng, Guo Jintian, Gao Wenjing, Li Bin, Shang Xin, Zheng Li, Wu Bin, Fu Yinghua

机构信息

Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi 830017, China.

Institute of Agro-Products Storage and Processing, Xinjiang Academy of Agricultural Sciences, Urumqi 830091, China.

出版信息

Foods. 2025 Jan 2;14(1):108. doi: 10.3390/foods14010108.

Abstract

Dried apricots are rich in a variety of polyphenols, which have anti-cancer activity. In this study, 949 phenolic substances were found by means of UPLC-MS/MS, mainly including 2',7-dihydroxy-3',4'-dimethoxyisoflavan, scopoletin, rutin, quercetin-3-O-robinobioside, and elaidolinolenic acid. The results indicated that dried apricot polyphenols (DAPs) could cause cell cycle arrest in the G0/G1 and G2/M phases by decreasing the cyclin D1, CDK4, cyclin B1, CDK1, and CDK6 levels in A549 human lung adenocarcinoma cells. Moreover, the ROS and Bax levels were increased, and the Bcl-2 and mitochondrial membrane potential were decreased in A549 cells treated with DAP, increasing caspase-9, caspase-3, and cleaved-PARP1 activities and leading to apoptosis of the A549 cells. Meanwhile, tumor growth was also inhibited by DAPs in an A549 tumor-bearing mouse model, Bax and caspase-3 were upregulated, and Bcl-2 was downregulated, inducing apoptosis of lung cancer cells. In conclusion, DAPs could inhibit lung cancer cell growth by inducing apoptosis due to cell cycle arrest and mitochondria-dependent pathways.

摘要

杏干富含多种具有抗癌活性的多酚类物质。在本研究中,通过超高效液相色谱-串联质谱法检测到949种酚类物质,主要包括2',7-二羟基-3',4'-二甲氧基异黄酮、东莨菪亭、芦丁、槲皮素-3-O-刺槐二糖苷和反式亚麻酸。结果表明,杏干多酚(DAPs)可通过降低A549人肺腺癌细胞中细胞周期蛋白D1、细胞周期蛋白依赖性激酶4(CDK4)、细胞周期蛋白B1、细胞周期蛋白依赖性激酶1(CDK1)和细胞周期蛋白依赖性激酶6(CDK6)的水平,使细胞周期停滞在G0/G1期和G2/M期。此外,用DAP处理的A549细胞中活性氧(ROS)和Bax水平升高,Bcl-2和线粒体膜电位降低,半胱天冬酶-9、半胱天冬酶-3和裂解的聚(二磷酸腺苷-核糖)聚合酶1(cleaved-PARP1)的活性增加,导致A549细胞凋亡。同时,在A549荷瘤小鼠模型中,DAPs也抑制了肿瘤生长,上调了Bax和半胱天冬酶-3,下调了Bcl-2,诱导肺癌细胞凋亡。总之,DAPs可通过细胞周期停滞和线粒体依赖性途径诱导细胞凋亡,从而抑制肺癌细胞生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a67/11719503/e769da3e2cbd/foods-14-00108-g001.jpg

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