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CJAP ›› 2019, Vol. 35 ›› Issue (4): 289-292.doi: 10.12047/j.cjap.5741.2019.060

• ORIGINAL ARTICLES •     Next Articles

The effects of Sestrin2 on apoptosis of heat-exposed lung epithelial cells and its mechanism

GAO Xiu-jie+, WANG Shang+, LIU Wei-li, WANG Kun, CHEN Zhao-li, WANG Xin-xing   

  1. Environmental Medicine Laboratory, Institute of Environmental and Operational Medicine, Academy of Military Medical Sciences, Tianjin 300050, China
  • Received:2018-08-27 Online:2019-07-28 Published:2019-11-06

Abstract: Objective: To investigate the protective effects of Sestrin2 protein on lung epithelial Beas-2B cells in the heat-exposure environment and its mechanism. Methods: Lung epithelial Beas-2B cells were cultured at 37℃, 39℃, 40℃ and 41℃ respectively. Cells were harvested at different times (0, 3, 6 and 12 h) after pancreatin digestion. The expressions of Sestrin2, superoxide dismutase(SOD), reactive oxygen species(ROS), cell mitochondrial membrane potential and apoptosis rate of cells were detected by Western blot, fluorescence spectrophotometer and flow cytometry, respectively. Gene expression sequence was cloned into high expression plasmid pcDNA3.1+. Beas-2B cells were transfected by Lipfectamine 2000 to construct Sestrin2 and SOD high expression cells. The changes of mitochondrial membrane potential and cell apoptosis were observed in the Sestrin2 and SOD high expression cells. Results: With the increase of temperature, the expression level of Sestrin2 protein in heat treatment group was decreased compared with the control group. When Beas-2B cells were exposed to 41℃, the ROS level was increased, mitochondrial membrane potential was decreased significantly and apoptosis rate was increased at different time points. After high expression of Sestrin2 and SOD in the Beas-2B cells, the expression level of ROS was decreased and the change tendency of mitochondrial membrane potential was decreased, and the apoptosis rate was reduced at 41℃ exposure. Conclusion: Sestrin2 can alleviate the apoptosis of lung epithelial cells induced by heat exposure through mitochondrial membrane potential and SOD, which has protective effect on lung epithelial Beas-2B cells.

Key words: Sestrin2, heat exposure, oxidative stress, apoptosis

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