Chattopadhyay Sourav, Dash Sandeep Kumar, Tripathy Satyajit, Das Balaram, Kar Mahapatra Santanu, Pramanik Panchanan, Roy Somenath
Immunology and Microbiology Laboratory, Department of Human Physiology with Community Health, Vidyasagar University, Midnapore, -721 102, West Bengal, India.
J Appl Toxicol. 2015 Jun;35(6):603-13. doi: 10.1002/jat.3080. Epub 2015 Jan 11.
The purpose of this study was to determine the intracellular signaling transduction pathways involved in oxidative stress induced by nanoparticles in cancer cells. Activation of reactive oxygen species (ROS) has some therapeutic benefits in arresting the growth of cancer cells. Cobalt oxide nanoparticles (CoO NPs) are an interesting compound for oxidative cancer therapy. Our results showed that CoO NPs elicited a significant (P <0.05) amount of ROS in cancer cells. Co-treatment with N-aceyltine cystine (an inhibitor of ROS) had a protective role in cancer cell death induced by CoO NPs. In cultured cells, the elevated level of tumor necrosis factor-alpha (TNF-α) was noted after CoO NPs treatment. This TNF-α persuaded activation of caspase-8 followed by phosphorylation of p38 mitogen-activated protein kinase and induced cell death. This study showed that CoO NPs induced oxidative stress and activated the signaling pathway of TNF-α-Caspase-8-p38-Caspase-3 to cancer cells.
本研究的目的是确定参与纳米颗粒诱导癌细胞氧化应激的细胞内信号转导途径。活性氧(ROS)的激活在抑制癌细胞生长方面具有一些治疗益处。氧化钴纳米颗粒(CoO NPs)是用于氧化癌症治疗的一种有趣化合物。我们的结果表明,CoO NPs在癌细胞中引发了显著(P<0.05)量的ROS。与N-乙酰半胱氨酸(一种ROS抑制剂)共同处理对CoO NPs诱导的癌细胞死亡具有保护作用。在培养细胞中,CoO NPs处理后观察到肿瘤坏死因子-α(TNF-α)水平升高。这种TNF-α促使半胱天冬酶-8激活,随后p38丝裂原活化蛋白激酶磷酸化并诱导细胞死亡。本研究表明,CoO NPs诱导氧化应激并激活癌细胞中TNF-α-半胱天冬酶-8-p38-半胱天冬酶-3信号通路。