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大戟因子L2通过线粒体途径诱导A549细胞凋亡。

Euphorbia factor L2 induces apoptosis in A549 cells through the mitochondrial pathway.

作者信息

Lin Minting, Tang Sili, Zhang Chao, Chen Hubiao, Huang Wenjing, Liu Yun, Zhang Jianye

机构信息

School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou 510182, China.

School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.

出版信息

Acta Pharm Sin B. 2017 Jan;7(1):59-64. doi: 10.1016/j.apsb.2016.06.008. Epub 2016 Jul 30.

DOI:10.1016/j.apsb.2016.06.008
PMID:28119809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5237708/
Abstract

Euphorbia factor L2, a lathyrane diterpenoid isolated from caper euphorbia seed (the seeds of L.), has been traditionally applied to treat cancer. This article focuses on the cytotoxic activity of Euphorbia factor L2 against lung carcinoma A549 cells and the mechanism by which apoptosis is induced. We analyzed the cytotoxicity and related mechanism of Euphorbia factor L2 with an MTT assay, an annexin V-FITC/PI test, a colorimetric assay, and immunoblotting. Euphorbia factor L2 showed potent cytotoxicity to A549 cells. Euphorbia factor L2 led to an increase in reactive oxygen species (ROS) generation, a loss of mitochondrial electrochemical potential, release of cytochrome activation of caspase-9 and caspase-3, and cleavage of poly(ADP-ribose) polymerase, suggesting that Euphorbia factor L2 induced apoptosis through a mitochondrial pathway. The cytotoxic activity of Euphorbia factor L2 in A549 cells and the related mechanisms of apoptotic induction provide support for the further investigation of caper euphorbia seeds.

摘要

大戟因子L2是从续随子（大戟科植物续随子的种子）中分离出的一种瑞香烷二萜类化合物，传统上被用于治疗癌症。本文重点研究大戟因子L2对肺癌A549细胞的细胞毒性活性及其诱导细胞凋亡的机制。我们通过MTT法、膜联蛋白V-FITC/PI检测、比色法和免疫印迹分析了大戟因子L2的细胞毒性及相关机制。大戟因子L2对A549细胞显示出强大的细胞毒性。大戟因子L2导致活性氧（ROS）生成增加、线粒体电化学电位丧失、细胞色素释放、半胱天冬酶-9和半胱天冬酶-3激活以及聚（ADP-核糖）聚合酶裂解，表明大戟因子L2通过线粒体途径诱导细胞凋亡。大戟因子L2在A549细胞中的细胞毒性活性及凋亡诱导的相关机制为进一步研究续随子种子提供了支持。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/4e4161883c00/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/850c9c2dba19/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/0a1131235346/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/c01ec9557c85/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/1e5724e23745/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/80447a27b3eb/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/ffaa5100aed3/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/4e4161883c00/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/850c9c2dba19/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/0a1131235346/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/c01ec9557c85/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/1e5724e23745/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/80447a27b3eb/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/ffaa5100aed3/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca05/5237708/4e4161883c00/gr6.jpg

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