Li Shufang,Huang Liqun,Yuan Yayi,et al.Mechanism of the protective effect of mild hypothermia on acute radiation injury in mice[J].Chinese Journal of Radiological Medicine and Protection,2015,35(5):339-343 |
Mechanism of the protective effect of mild hypothermia on acute radiation injury in mice |
Received:August 13, 2014 |
DOI:10.3760/cma.j.issn.0254-5098.2015.05.005 |
KeyWords:Mild hypothermia Acute radiation injury Protective effect |
FundProject:山西省实验动物专项资金项目(2013k07) |
Author Name | Affiliation | E-mail | Li Shufang | China Institute for Radiation Protection, Shanxi Key Laboratory of Drug Toxicology and Drug for Radiation Injury, Taiyuan 030006, China | | Huang Liqun | China Institute for Radiation Protection, Shanxi Key Laboratory of Drug Toxicology and Drug for Radiation Injury, Taiyuan 030006, China | | Yuan Yayi | China Institute for Radiation Protection, Shanxi Key Laboratory of Drug Toxicology and Drug for Radiation Injury, Taiyuan 030006, China | | Sun Ge | China Institute for Radiation Protection, Shanxi Key Laboratory of Drug Toxicology and Drug for Radiation Injury, Taiyuan 030006, China | | Liu Hongyan | China Institute for Radiation Protection, Shanxi Key Laboratory of Drug Toxicology and Drug for Radiation Injury, Taiyuan 030006, China | | Wang Yongli | China Institute for Radiation Protection, Shanxi Key Laboratory of Drug Toxicology and Drug for Radiation Injury, Taiyuan 030006, China | | Yue Juan | China Institute for Radiation Protection, Shanxi Key Laboratory of Drug Toxicology and Drug for Radiation Injury, Taiyuan 030006, China | | Wen Jianhua | China Institute for Radiation Protection, Shanxi Key Laboratory of Drug Toxicology and Drug for Radiation Injury, Taiyuan 030006, China | | Zhang Wei | China Institute for Radiation Protection, Shanxi Key Laboratory of Drug Toxicology and Drug for Radiation Injury, Taiyuan 030006, China | | An Quan | China Institute for Radiation Protection, Shanxi Key Laboratory of Drug Toxicology and Drug for Radiation Injury, Taiyuan 030006, China | anquan@cirp.org.cn |
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Abstract:: |
Objective To explore the effect of mild hypothermia on acute radiation injury in mice and investigate the underlying mechanism. Methods Totally 105 BALB/c mice were randomly divided into 3 groups of equal number: irradiation group, mild hypothermia prevention group and normal control group. Mice in groups of irradiation and mild hypothermia prevention were administered with whole body irradiation of 6 Gy γ-rays, mice in irradiation group were treated with mild hypothermia after irradiation immediately and maintenance for 6 h. White blood cells, nucleated cells and histopathological changes in bone marrow were observed at 1, 3, 7, 14, 21 and 28 d after irradiation. At 6 and 24 h after irradiation, the content of malondiadehyde (MDA) and the activities of superoxide dismutase enzyme (SOD) and glutathione peroxidase enzyme (GSH-px) in serum were detected, and the cell cycle distribution of bone marrow cells were also measured with flow cytometry. Results The numbers of white blood cell and nucleated cells in bone marrow in mild hypothermia prevention group were much higher than those in irradiation group (t=-2.63,-3.41,P<0.05) at the early period after irradiation so that they were recovered 1 week earlier. Pathology measurement showed that cells in bone marrow of mild hypothermia prevention group decayed later and recovered 1 week earlier than irradiation group. At 6 h after irradiation, in mild hypothermia prevention group, MDA content was lower (t=3.83,P<0.05) and the activity of SOD was higher (t=-6.57,P<0.05) than that in irradiation group, meanwhile, the S-phase cells in bone marrow were higher (t=-4.67,P<0.05) and the G2-phase cells were lower (t=3.04, P<0.05) than those of irradiation group. At 24 h after irradiation, for mild hypothermia prevention group, the activity of GSH-px was higher (t=-3.13, P<0.05) and the S-phase cells in bone marrow was lower (t=7.19, P<0.05) than those in irradiation group. Conclusions Mild hypothermia has protective effect on acute radiation injury by enhancing the antioxidant capacity and inhibiting bone marrow cell cycle progress. |
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