标题：Probucol protects circulating endothelial progenitor cells from ambient PM2.5 damage via inhibition of reactive oxygen species and inflammatory cytokine production in vivo
作者：Chen, Yong; Hu, Ke; Bu, Haoran; Si, Zhihua; Sun, Haihui; Chen, Liming; Liu, Hang; Xie, Hao; Zhao, Peng; Yang, Le; Sun, Qinghua; 更多 作者机构：[Chen, Yong; Bu, Haoran] Shandong Univ, Shandong Prov Hosp, Dept Emergency, Jinan 250021, Shandong, Peoples R China.; [Hu, Ke] Shandong Univ, Qianfo 更多
通讯作者：Cui, LQ;Cui, YQ
通讯作者地址：[Cui, LQ; Cui, YQ]Shandong Univ, Shandong Prov Hosp, Dept Cardiol, 324 Jingwuweiqi Rd, Jinan 250021, Shandong, Peoples R China.
来源：EXPERIMENTAL AND THERAPEUTIC MEDICINE
关键词：probucol; endothelial progenitor cells; PM2; 5; reactive oxygen species;; inflammatory cytokines
摘要：Bone marrow-derived circulating endothelial progenitor cells (EPCs) contribute to angiogenesis and vascular repair. The number and function of EPCs are significantly decreased following exposure to ambient fine particulate matter of 2.5 mu m in diameter (PM2.5) through reactive oxygen species (ROS) generation and inflammatory cytokine secretion. The anti-oxidant drug probucol reduces ROS and inflammatory cytokine production. The present study was designed to determine the protective effects of probucol on EPCs from PM2.5-associated impairment in vivo and to explore the potential underlying mechanisms. Male C57BL/6 mice were exposed to ambient air containing PM2.5 for one month with or without probucol treatment. Mice that breathed filtered air were used as a control group. Serum and blood cells were collected for analysis. The results indicated that PM2.5 exposure induced increases in blood intracellular ROS, serum inflammatory cytokine levels and the blood cell apoptotic rate, while it decreased the number and proliferation rate of circulating EPCs in the mice with PM2.5 exposure. These effects were significantly reduced/abrogated by probucol treatment. The present in vivo study suggested that probucol protects EPCs from damage through PM2.5 exposure by inhibiting ROS generation and inflammatory cytokine production.