| Liu Lang,Liu Dengqun,Wang Yu,Wang Ziwen,Chen Zelin,Chen Jie,Han Xiao,Liu Zujuan,Zhang Aihua,Shi Chunmeng.Enhanced autophagy protects hepatic cells from radiation injury[J].中华放射医学与防护杂志,2018,38(5):335-343 |
| Enhanced autophagy protects hepatic cells from radiation injury |
| Enhanced autophagy protects hepatic cells from radiation injury |
| 投稿时间：2017-12-14 |
| DOI：10.3760/cma.j.issn.0254-5098.2018.05.003 |
| 中文关键词: Autophagy Radiation Hepatic cells Apoptosis ROS |
| 英文关键词:Autophagy Radiation Hepatic cells Apoptosis ROS |
| 基金项目:National Key Research and Development Program (2016YFC1000805);National Natural Science Foundation of China (81371688,81673089);University Innovation Team Building Program of Chongqing (CXTDG201602020);Intramural Research Project Grants (BWS13C016 and AWS14007-01);Chongqing Science and Technology Commission (cstc2013jcyjA10038) |
| 作者 | 单位 | E-mail | | Liu Lang | Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Department of Toxicology, Guizhou Medical University, Guiyang 550025, China | | | Liu Dengqun | State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400038, China | | | Wang Yu | State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400038, China | | | Wang Ziwen | State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400038, China | | | Chen Zelin | State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400038, China | | | Chen Jie | State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400038, China | | | Han Xiao | State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400038, China | | | Liu Zujuan | State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400038, China | | | Zhang Aihua | Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Department of Toxicology, Guizhou Medical University, Guiyang 550025, China | aihuagzykd@163.com | | Shi Chunmeng | State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400038, China | shicm@sina.com |
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| 中文摘要: |
| Objective To study the influence of radiation on autophagy and its protective effect on radiation injury of hepatic cells. Methods Autophagy in mouse liver tissues was examined by GFP-LC3 staining and Western blot. Radiation-induced hepatic injury was evaluated by ALT and AST in mouse serum, protein expressions, and H & E and TUNEL staining of liver tissue. L02 cells were used for in vitro study. Chloroquine and rapamycin were used to manipulate the level of autophagy. Results Total body irradiation (TBI) of 8 Gy caused an increase of autophagy in mouse liver tissue and AST level in serum(t=-7.47, P<0.05) at 12 h after irradiation. Irradiation significantly increased the apoptotic level in liver tissue as well. Inhibition of autophagy by chloroquine caused a further increases of AST[IR:(345.42±35.25)U/L vs. IR+CQ:(433.42±40.07)U/L, t=-2.86, P<0.05] and ALT[IR:(35.67±8.08)U/L vs. IR+CQ:(98.5±26.67)U/L, t=-3.09, P<0.05] in the serum, and it also promoted apoptosis in live tissue. However, rapamycin as an autophagy promoter showed protective effect for radiation-induced hepatic injury[AST:IR:(345.42±35.25)U/L vs. IR+Rap:(278.42±20.09)U/L, t=-2.86, P<0.05]. Similar changes of autophagy and apoptosis in L02 cells were also observed in the cells treated with chloroquine and rapamycin. Inhibition of autophagy by CQ caused an increase of ROS in vitro and in vivo and further increased ALT and AST levels in serum, reduced L02 cell viability. Activation of autophagy by Rap effectively reversed those changes. Conclusions Autophagy protects hepatic cells from radiation injury by decreasing ROS induction, which provides a potential target for the development of new clinical regimens against radiation induced liver injury. |
| 英文摘要: |
| Objective To study the influence of radiation on autophagy and its protective effect on radiation injury of hepatic cells. Methods Autophagy in mouse liver tissues was examined by GFP-LC3 staining and Western blot. Radiation-induced hepatic injury was evaluated by ALT and AST in mouse serum, protein expressions, and H & E and TUNEL staining of liver tissue. L02 cells were used for in vitro study. Chloroquine and rapamycin were used to manipulate the level of autophagy. Results Total body irradiation (TBI) of 8 Gy caused an increase of autophagy in mouse liver tissue and AST level in serum(t=-7.47, P<0.05) at 12 h after irradiation. Irradiation significantly increased the apoptotic level in liver tissue as well. Inhibition of autophagy by chloroquine caused a further increases of AST[IR:(345.42±35.25)U/L vs. IR+CQ:(433.42±40.07)U/L, t=-2.86, P<0.05] and ALT[IR:(35.67±8.08)U/L vs. IR+CQ:(98.5±26.67)U/L, t=-3.09, P<0.05] in the serum, and it also promoted apoptosis in live tissue. However, rapamycin as an autophagy promoter showed protective effect for radiation-induced hepatic injury[AST:IR:(345.42±35.25)U/L vs. IR+Rap:(278.42±20.09)U/L, t=-2.86, P<0.05]. Similar changes of autophagy and apoptosis in L02 cells were also observed in the cells treated with chloroquine and rapamycin. Inhibition of autophagy by CQ caused an increase of ROS in vitro and in vivo and further increased ALT and AST levels in serum, reduced L02 cell viability. Activation of autophagy by Rap effectively reversed those changes. Conclusions Autophagy protects hepatic cells from radiation injury by decreasing ROS induction, which provides a potential target for the development of new clinical regimens against radiation induced liver injury. |
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