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PUMA和生存素通过线粒体介导的途径参与微囊藻毒素-LR诱导的HepG2细胞凋亡。

PUMA and survivin are involved in the apoptosis of HepG2 cells induced by microcystin-LR via mitochondria-mediated pathway.

作者信息

Ma Junguo, Feng Yiyi, Liu Yang, Li Xiaoyu

机构信息

College of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.

College of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.

出版信息

Chemosphere. 2016 Aug;157:241-9. doi: 10.1016/j.chemosphere.2016.05.051. Epub 2016 May 26.

Abstract

The present study aimed to determine the cytotoxicity of microcystin-LR (MC-LR) on the human hepatocellular carcinoma (HepG2) cells in order to elucidate the mechanism of apoptosis induced by MC-LR. Morphological evaluation results showed that MC-LR induced time- and concentration-dependent apoptosis in HepG2 cells. The biochemical assays revealed that MC-LR-exposure caused overproduction of reactive oxygen species (ROS), cyclooxygenase-2 activity alteration, cytochrome c release, and remarkable activation of caspase-3 and caspase-9 in HepG2 cells, indicating that MC-LR-induced apoptosis is mediated by mitochondrial pathway. Moreover, we also found that p53 and Bax might play an important role in MC-LR-induced apoptosis in HepG2 cells in which PUMA and survivin were involved. However, further studies are necessary to elucidate the possible functions of PUMA and survivin in MC-LR-induced apoptosis in HepG2 cells.

摘要

本研究旨在确定微囊藻毒素-LR(MC-LR)对人肝癌(HepG2)细胞的细胞毒性,以阐明MC-LR诱导细胞凋亡的机制。形态学评估结果显示,MC-LR诱导HepG2细胞发生时间和浓度依赖性凋亡。生化分析表明,暴露于MC-LR会导致HepG2细胞中活性氧(ROS)过量产生、环氧合酶-2活性改变、细胞色素c释放以及半胱天冬酶-3和半胱天冬酶-9显著激活,表明MC-LR诱导的细胞凋亡是由线粒体途径介导的。此外,我们还发现p53和Bax可能在MC-LR诱导的HepG2细胞凋亡中起重要作用,其中PUMA和生存素也参与其中。然而,需要进一步研究以阐明PUMA和生存素在MC-LR诱导的HepG2细胞凋亡中的可能作用。

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