Probucol protects circulating endothelial progenitor cells from ambient PM(2.5) damage via inhibition of reactive oxygen species and inflammatory cytokine production in vivo

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 µm in diameter (PM(2.5)) 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 PM(2.5)-associated impairment in vivo and to explore the potential underlying mechanisms. Male C57BL/6 mice were exposed to ambient air containing PM(2.5) 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 PM(2.5) 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 PM(2.5) exposure. These effects were significantly reduced/abrogated by probucol treatment. The present in vivo study suggested that probucol protects EPCs from damage through PM(2.5) exposure by inhibiting ROS generation and inflammatory cytokine production.