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首页> 美国卫生研究院文献>Cytotechnology >2′4′-Dihydroxy-6′-methoxy-3′5′-dimethylchalcone from buds of Cleistocalyx operculatus induces apoptosis in human hepatoma SMMC-7721 cells through a reactive oxygen species-dependent mechanism
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2′4′-Dihydroxy-6′-methoxy-3′5′-dimethylchalcone from buds of Cleistocalyx operculatus induces apoptosis in human hepatoma SMMC-7721 cells through a reactive oxygen species-dependent mechanism

机译：盖草芽中的24-二羟基-6-甲氧基-35-二甲基查尔酮通过反应性氧依赖机制诱导人肝癌SMMC-7721细胞凋亡

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Nowadays, much effort is being devoted to detect new substances that not only significantly induce the death of tumor cells, but also have little side effect on normal cells. Our previous study showed that 2′,4′-dihydroxy-6′-methoxy-3′,5′-dimethylchalcone (DMC) exhibited significant cytotoxic potential with an IC50 value of 32.3 ± 1.13 μM against SMMC-7721 cells and could induce SMMC-7721 cells apoptosis. In the present study, we found that DMC was almost nontoxic to human normal liver L-02 and human normal fetal lung fibroblast HFL-1 cells as their IC50 values (111.0 ± 4.57 and 152.0 ± 4.83 µM for L-02 and HFL-1 cells, respectively) were much higher. To further explore the apoptotic mechanism of DMC, we investigated the role of the reactive oxygen species (ROS) in the apoptosis induced by DMC in SMMC-7721 cells. Our results suggested that the cytotoxicity and the generation of intracellular ROS were inhibited by N-acetylcysteine (NAC). Reversal of apoptosis in NAC pretreated cells indicated the involvement of ROS in DMC-induced apoptosis. The loss of mitochondrial membrane potential (ΔΨm) induced by DMC was significantly blocked by NAC. NAC also prevented the decrease of Caspase-3 and -9 activities, the increase of Bcl-2 protein expression and the decrease of p53 and PUMA protein expressions. Together, these results indicated that ROS played a key role in the apoptosis induced by DMC in human hepatoma SMMC-7721 cells.
机译：如今，人们正在付出巨大的努力来检测不仅能显着诱导肿瘤细胞死亡，而且对正常细胞几乎没有副作用的新物质。我们之前的研究表明，2'，4'-二羟基-6'-甲氧基-3'，5'-二甲基查尔酮（DMC）对SMMC-7721细胞具有显着的细胞毒性潜力，IC50值为32.3±1.13μM，可以诱导SMMC -7721细胞凋亡。在本研究中，我们发现DMC对人正常的肝L-02和人正常的胎儿肺成纤维细胞HFL-1细胞几乎无毒，因为它们的IC50值（L-02和HFL-1为111.0±4.57和152.0±4.83μM个单元格）要高得多。为了进一步探索DMC的凋亡机制，我们研究了活性氧（ROS）在DMC诱导SMMC-7721细胞凋亡中的作用。我们的结果表明，N-乙酰半胱氨酸（NAC）抑制了细胞毒性和细胞内ROS的产生。 NAC预处理细胞的凋亡逆转表明ROS参与了DMC诱导的细胞凋亡。 NAC明显阻止了DMC引起的线粒体膜电位（ΔΨm）的损失。 NAC还阻止了Caspase-3和-9活性的降低，Bcl-2蛋白表达的提高以及p53和PUMA蛋白表达的降低。总之，这些结果表明ROS在人肝癌SMMC-7721细胞中由DMC诱导的凋亡中起关键作用。

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