Probucol protects circulating endothelial progenitor cells from ambient PM2.5 damage via inhibition of reactive oxygen species and inflammatory cytokine production in vivo
Autor: | Hao Xie, Zhenguo Liu, Le Yang, Yuqi Cui, Yong Chen, Haoran Bu, Zhihua Si, Ke Hu, Peng Zhao, Lianqun Cui, Haihui Sun, Hang Liu, Liming Chen, Qinghua Sun |
---|---|
Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Cancer Research Angiogenesis inflammatory cytokines medicine.medical_treatment Probucol probucol PM2.5 Pharmacology complex mixtures Proinflammatory cytokine Blood cell 03 medical and health sciences 0302 clinical medicine Immunology and Microbiology (miscellaneous) medicine Progenitor cell endothelial progenitor cells chemistry.chemical_classification reactive oxygen species Reactive oxygen species General Medicine Articles 030104 developmental biology medicine.anatomical_structure Cytokine chemistry 030220 oncology & carcinogenesis Cytokine secretion medicine.drug |
Zdroj: | Experimental and Therapeutic Medicine |
ISSN: | 1792-1015 1792-0981 |
Popis: | 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 (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. |
Databáze: | OpenAIRE |
Externí odkaz: | |
Nepřihlášeným uživatelům se plný text nezobrazuje | K zobrazení výsledku je třeba se přihlásit. |