Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 44, Issue 4, Pages 1629-1639Publisher
KARGER
DOI: 10.1159/000485762
Keywords
Taurine; Ionizing radiation; GC-2 cells; Nrf2/HO-1 signaling
Categories
Funding
- National Key Basic Research Program (973 project) from the Ministry of Science and Technology of China [2015CB554004]
- National Natural Science Foundation of China [81372240, 81672775, 81330037]
- Natural Science Foundation of Shanghai [14JC1407800, 15XD1504500]
Ask authors/readers for more resources
Background/Aims: The increasing prevalence of ionizing radiation exposure has inevitably raised public concern over the potential detrimental effects of ionizing radiation on male reproductive system function. The detection of drug candidates to prevent reproductive system from damage caused by ionizing radiation is urgent. We aimed to investigate the protective role of taurine on the injury of mouse spermatocyte-derived cells (GC-2) subjected to ionizing radiation. Methods: mouse spermatocytes (GC-2 cells) were exposed to ionizing radiation with or without treatment of Taurine. The effect of ionizing radiation and Taurine treatment on GC-2 cells were evaluated by cell viability assay (CCK8), cell cycle and apoptosis. The relative protein abundance change was determined by Western blotting. The siRNA was used to explore whether Nrf2 signaling was involved in the cytoprotection of Taurine. Results: Taurine significantly inhibited the decrease of cell viability, percentage of apoptotic cells and cell cycle arrest induced by ionizing radiation. Western blot analysis showed that taurine significantly limited the ionizing radiation-induced down-regulation of CyclinB1 and CDK1, and suppressed activation of Fas/FasL system pathway. In addition, taurine treatment significantly increased the expression of Nrf2 and HO-1 in GC-2 cells exposed to ionizing radiation, two components in antioxidant pathway. The above cytoprotection of Taurine was blocked by siNrf2. Conclusion: Our results demonstrate that taurine has the potential to effectively protect GC-2 cells from ionizing radiation-triggered damage via upregulation of Nrf2/HO-1 signaling. (C) 2017 The Author(s) Published by S. Karger AG, Basel
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available