Research Paper Volume 12, Issue 16 pp 16368—16389
Flavonoids from Rosa roxburghii Tratt prevent reactive oxygen species-mediated DNA damage in thymus cells both combined with and without PARP-1 expression after exposure to radiation in vivo
- 1 Department of Pharmacy, Xinxiang Medical University, Xinxiang 453003, Henan, China
- 2 College of Medical Laboratory, Xinxiang Medical University, Xinxiang 453003, Henan, China
- 3 Henan Key Laboratory of Medical Tissue Regeneration, Xinxiang Medical University, Xinxiang 453003, Henan, China
- 4 International Joint Research Laboratory for Recombinant Pharmaceutical Protein Expression System of Henan, Xinxiang Medical University, Xinxiang 453003, Henan, China
Received: September 16, 2019 Accepted: June 13, 2020 Published: August 29, 2020https://doi.org/10.18632/aging.103688
How to Cite
Copyright © 2020 Xu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This study aimed to evaluate the role of FRT in ROS/DNA regulation with or without PARP-1 in radiation-injured thymus cells. The administration of FRT to PARP-1-/- (KO) mice demonstrated that FRT significantly increased the viability of thymus cells and decreased their rate of apoptosis through PARP-1. Radiation increased the levels of ROS, γ-H2AX and 53BP1, and induced DNA double strand breaks. Compared with wild type (WT) mice, levels of ROS, γ-H2AX and 53BP1 in KO mice were much less elevated. The FRT treatment groups also showed little reduction in these indicators in KO mice compared with WT mice. The results of the KO mice study indicated that FRT reduced ROS activation through inhibition of PARP-1. Furthermore, FRT reduced the concentrations of γ-H2AX by decreasing ROS activation. However, we found that FRT did not regulate 53BP1, a marker of DNA damage, because of its elimination of ROS. Levels of apoptosis-inducing factor (AIF), exhibited no significant difference after irradiation in KO mice. To summarize, ROS suppression by PARP-1 knockout in KO mice highlights potential therapeutic target either by PARP-1 inhibition combined with radiation or by treatment with a drug therapy alone. AIF-induced apoptosis could not be activated in KO mice.