Protective Effect of Atorvastatin on Radiation-induced Vascular Endothelial Cell Injury In Vitro

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  • RAN Xin-Ze
    State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Combined Injury of PLA, College of Preventive Medicine, Third Military Medical University
  • RAN Xi
    Department of Laboratory Medicine, Xinqiao Hospital, Third Military Medical University
  • ZONG Zhao-Wen
    State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Combined Injury of PLA, College of Preventive Medicine, Third Military Medical University
  • LIU Deng-Qun
    State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Combined Injury of PLA, College of Preventive Medicine, Third Military Medical University
  • XIANG Gui-Ming
    Department of Laboratory Medicine, Xinqiao Hospital, Third Military Medical University
  • SU Yong-Ping
    State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Combined Injury of PLA, College of Preventive Medicine, Third Military Medical University
  • ZHENG Huai-En
    State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Combined Injury of PLA, College of Preventive Medicine, Third Military Medical University

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Vascular endothelial cells are very sensitive to ionizing radiation, and it is important to develop effective prevent agents and measures in radiation exposure protection. In the present study, the protective effects of atorvastatin on irradiated human umbilical vein endothelial cells (HUVEC) and the possible mechanisms were explored. Cultured HUVEC were treated by atorvastatin at a final concentration of 10 μ mol/ml for 10 minutes, and then irradiated at a dose of 2 Gy or 25 Gy. Twenty-four hours after irradiation, apoptosis of HUVEC was monitored by flow cytometry, and the expression of thrombomodulin (TM) and protein C activation in HUVEC was respectively assessed by flow cytometry and spectrophotometry. After treatment with atorvastatin for 24 h, the rate of cell apoptosis decreased by 6% and 16% in cells irradiated with 2 Gy and 25 Gy, respectively. TM expression increased by 77%, 59%, and 61% in untreated cells, 2 Gy irradiation-treated cells, and 25 Gy irradiation-treated cells, respectively. The protein C levels in 2 Gy and 25 Gy irradiation-treated cells were reduced by 23% and 34% when compared with untreated cells, but up-regulated by 79% and 76% when compared with cells which were irradiated and treated with atorvastatin. In conclusion, these data indicate that atorvastatin exerts protective effects on irradiated HUVEC by reducing apoptosis by up-regulating TM expression and enhancing protein C activation in irradiated HUVEC.

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