Deoxynivalenol inhibits proliferation and induces apoptosis in human umbilical vein endothelial cells

被引:21
|
作者
Deng, Chao [1 ]
Ji, Changyun [1 ]
Qin, Weisen [1 ]
Cao, Xifeng [1 ]
Zhong, Jialian [2 ]
Li, Yugu [2 ]
Srinivas, Swaminath [3 ]
Feng, Youjun [2 ]
Deng, Xianbo [1 ]
机构
[1] South China Agr Univ, Coll Vet Med, Guangzhou 510642, Guangdong, Peoples R China
[2] Zhejiang Univ, Sch Basic Med Sci, Ctr Infect & Immun, Hangzhou 310058, Zhejiang, Peoples R China
[3] Univ Illinois, Dept Biochem, Urbana, IL 61801 USA
关键词
Deoxynivalenol; HUVECs; Mitochondrial membrane potential; Cell cycle; Apoptosis; RIBOTOXIC STRESS-RESPONSE; ACTIVATED PROTEIN-KINASE; CYTOCHROME-C RELEASE; LEUKEMIA HL-60 CELLS; OXIDATIVE STRESS; FUSARIUM MYCOTOXINS; EPITHELIAL-CELLS; CACO-2; CELLS; CANCER CELLS; CYCLE ARREST;
D O I
10.1016/j.etap.2016.02.002
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Deoxynivalenol (DON) is astable mycotoxins found in cereals infected by certain fungal species and causes adverse health effects in animals and human such as vomiting, diarrhea and reproductive toxicity. In this study, we investigated the toxic and apoptotic effects of DON in human umbilical vein endothelial cells (HUVECs), a good model for studying inflammation. The results show that DON significantly inhibited the viability of HUVECs. DON could also inhibit the proliferation of HUVECs through G2/M phase arrest in cell cycle progression. Moreover, oxidative stress induced by DON was indicated by observations of increased levels of reactive oxygen species (ROS). In addition, DON also causes mitochondrial damage by decreasing the mitochondria( membrane potential and inducing apoptosis by up-regulation of apoptosis-related genes like caspase-3, caspase-9, and Sax genes, and down-regulation of Bcl-2 gene. These results together suggest that DON could induce cell cycle arrest, oxidative stress, and apoptosis in HUVECs. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:232 / 241
页数:10
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