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首页> 外文期刊>RSC Advances >Hydroxysafflor yellow A induces apoptosis in MCF-7 cells by blocking NF kappa B/p65 pathway and disrupting mitochondrial transmembrane potential
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Hydroxysafflor yellow A induces apoptosis in MCF-7 cells by blocking NF kappa B/p65 pathway and disrupting mitochondrial transmembrane potential

机译：羟基红花黄色素A通过阻断NFκB/ p65途径并破坏线粒体跨膜电位而诱导MCF-7细胞凋亡

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摘要

The molecular mechanisms and the possible effects of hydroxysafflor yellow A (HSYA) on the induction of apoptosis in the human breast cancer MCF-7 cells were investigated. The MTT assay showed that HSYA could specifically inhibit the growth of several solid tumor cells in a dose-dependent manner, especially in the MCF-7 cells. Analysis by flow cytometry indicated that the apoptosis of the MCF-7 cells increased after treatment with HSYA. Moreover, the ROS level increased, and the cell cycle was blocked when the MCF-7 cells were treated with HSYA. The HSYA-induced apoptosis involved Bax and p53 up-regulation, Bcl-2 and cyclin D1 down-regulation, release of cytochrome c from the mitochondria to the cytosol, activation of caspase-3, and disruption of the mitochondrial transmembrane potential (Delta psi(m)). In addition, HSYA could inhibit the NF kappa B/p65 pathway by blocking the NF kappa B/p65 nuclear translocation. We concluded that HSYA could induce apoptosis in MCF-7 cells and promote it through the mitochondrial apoptotic pathway.
机译：研究了羟基番红花黄A（HSYA）诱导人乳腺癌MCF-7细胞凋亡的分子机制和可能的作用。 MTT分析表明，HSYA可以剂量依赖性方式特异性抑制几种实体瘤细胞的生长，特别是在MCF-7细胞中。流式细胞仪分析表明，用HSYA处理后，MCF-7细胞的凋亡增加。此外，当用HSYA处理MCF-7细胞时，ROS水平增加，并且细胞周期被阻断。 HSYA诱导的凋亡涉及Bax和p53上调，Bcl-2和细胞周期蛋白D1下调，细胞色素c从线粒体释放到细胞质，激活caspase-3以及破坏线粒体跨膜电位（Δpsi）。 （m））。另外，HSYA可以通过阻断NFκB/ p65核易位而抑制NFκB/ p65通路。我们得出的结论是，HSYA可以诱导MCF-7细胞凋亡，并通过线粒体凋亡途径促进其凋亡。

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