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姜黄素通过氧化应激和丝裂原活化蛋白激酶(MAPK)信号通路诱导A549细胞凋亡。

Curcumin induces the apoptosis of A549 cells via oxidative stress and MAPK signaling pathways.

作者信息

Yao Qinghua, Lin Miao, Wang Yuqi, Lai Yuebiao, Hu Jingjing, Fu Ting, Wang Lu, Lin Shuyuan, Chen Liangliang, Guo Yong

机构信息

Key Laboratory of Traditional Chinese Medicine Oncology, Zhejiang Cancer Hospital, Banshan Qiao, Hangzhou, Zhejiang 310022, P.R. China.

Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P.R. China.

出版信息

Int J Mol Med. 2015 Oct;36(4):1118-26. doi: 10.3892/ijmm.2015.2327. Epub 2015 Aug 26.

DOI:10.3892/ijmm.2015.2327
PMID:26310655
Abstract

Curcumin has been found to exhibit anticancer activity and certain studies have shown that curcumin triggers the apoptosis of human A549 lung adenocarcinoma cells. However, the mechanism underlying curcumin‑mediated apoptosis is not completely understood. The present study was designed to investigate the effect of curcumin on the induction of apoptosis and apoptosis‑related factors in human A549 lung adenocarcinoma cells. Treatment of A549 cells with curcumin caused a concentration‑dependent inhibition of cell growth and an increase in apoptosis, as confirmed by THE MTT assay, flow cytometry and morphology analysis. Curcumin‑treatment of A549 cells induced a loss of the mitochondrial membrane potential and increased cytosolic cytochrome c. Furthermore, curcumin‑induced apoptosis was accompanied by changes in intracellular oxidative stress‑related enzymes, including decreased intracellular reactive oxygen species levels, increased superoxide dismutase and decreased malondialdehyde and 4‑hydroxynonenal. In addition, induction of apoptosis was also accompanied by phosphorylation and activation of mitogen‑activated protein kinase signaling pathway factors c‑Jun N‑terminal kinase, p38 and extracellular signal-regulated kinase.

摘要

姜黄素已被发现具有抗癌活性,并且某些研究表明姜黄素可触发人A549肺腺癌细胞的凋亡。然而,姜黄素介导凋亡的潜在机制尚未完全明确。本研究旨在探讨姜黄素对人A549肺腺癌细胞凋亡诱导及凋亡相关因子的影响。用姜黄素处理A549细胞导致细胞生长呈浓度依赖性抑制且凋亡增加,这通过MTT法、流式细胞术和形态学分析得以证实。用姜黄素处理A549细胞可诱导线粒体膜电位丧失并增加胞质细胞色素c。此外,姜黄素诱导的凋亡伴随着细胞内氧化应激相关酶的变化,包括细胞内活性氧水平降低、超氧化物歧化酶增加以及丙二醛和4-羟基壬烯醛减少。另外,凋亡的诱导还伴随着丝裂原活化蛋白激酶信号通路因子c-Jun氨基末端激酶、p38和细胞外信号调节激酶的磷酸化和激活。

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