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姜黄素通过调节线粒体信号通路诱导SGC-7901胃腺癌细胞凋亡。

Curcumin induces apoptosis in SGC-7901 gastric adenocarcinoma cells via regulation of mitochondrial signaling pathways.

作者信息

Xue Xia, Yu Jin-Long, Sun De-Qing, Kong Feng, Qu Xian-jun, Zou Wen, Wu Jing, Wang Rong-Mei

机构信息

Department of Pharmacy, The Second Hospital of Shandong University, Jinan, China E-mail :

出版信息

Asian Pac J Cancer Prev. 2014;15(9):3987-92. doi: 10.7314/apjcp.2014.15.9.3987.

DOI:10.7314/apjcp.2014.15.9.3987
PMID:24935585
Abstract

Curcumin, a polyphenol compound derived from the rhizome of the plant Curcuma longa L. has been verified as an anticancer compound against several types of cancer. However, understanding of the molecular mechanisms by which it induces apoptosis is limited. In this study, the anticancer efficacy of curcumin was investigated in human gastric adenocarcinoma SGC-7901 cells. The results demonstrated that curcumin induced morphological changes and decreased cell viability. Apoptosis triggered by curcumin was visualized using Annexin V-FITC/7- AAD staining. Curcumin-induced apoptosis of SGC-7901 cells was associated with the dissipation of mitochondrial membrane potential (MMP) and the release of cytochrome c into the cytosol. Furthermore, the down-regulation of Bcl-2 and up-regulation of Bax that led to the cleavage of caspase-3 and increased cleaved PARP was observed in SGC-7901 cells treated with curcumin. Therefore, curcumin-induced apoptosis of SGC-7901 cells might be mediated through the mitochondria pathway, which gives the rationale for in vivo studies on the utilization of curcumin as a potential cancer therapeutic compound.

摘要

姜黄素是一种从植物姜黄的根茎中提取的多酚化合物,已被证实是一种针对多种癌症的抗癌化合物。然而,对于其诱导细胞凋亡的分子机制的了解还很有限。在本研究中,研究了姜黄素对人胃腺癌SGC - 7901细胞的抗癌效果。结果表明,姜黄素可诱导细胞形态变化并降低细胞活力。使用膜联蛋白V - FITC/7 - AAD染色观察姜黄素引发的细胞凋亡。姜黄素诱导SGC - 7901细胞凋亡与线粒体膜电位(MMP)的消散以及细胞色素c释放到细胞质中有关。此外,在用姜黄素处理的SGC - 7901细胞中,观察到Bcl - 2下调和Bax上调,这导致了caspase - 3的裂解以及裂解的PARP增加。因此,姜黄素诱导SGC - 7901细胞凋亡可能是通过线粒体途径介导的,这为姜黄素作为一种潜在的癌症治疗化合物的体内研究提供了理论依据。

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