Journal
JOURNAL OF ASSISTED REPRODUCTION AND GENETICS
Volume 38, Issue 9, Pages 2349-2361Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10815-021-02229-7
Keywords
Implantation; Oxidative stress; Sirtuin-1; FoxO1; SOD
Funding
- Scientific Research Projects Coordination Unit of Akdeniz University [TYL-2017-2427]
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This study suggests that sirtuin-1 may play a role in embryo implantation against oxidative stress through FoxO1-SOD signaling. In SRT1720-treated mice, expressions of sirtuin-1 and FoxO1 increased at implantation sites, while ROS/RNS levels decreased and SOD activity increased.
Purpose Implantation is essential for a successful pregnancy. Despite the increasing number of studies, implantation is still an unknown process. This study aimed to determine whether sirtuin-1 has a role in embryo implantation in oxidative stress-induced mice. Methods Pregnant mice were separated into 5 groups: control, vehicle, paraquat, SRT1720, and SRT1720+Paraquat. Paraquat is a herbicide and is used to induce oxidative stress. SRT1720 is a specific sirtuin-1 activator. Implantation and inter-implantation sites were removed in the morning of the 5th day of pregnancy after Chicago blue injection was performed. Sirtuin-1 and Forkhead box O1 (FoxO1) were detected by immunohistochemistry and Western blot while acetylated lysine was evaluated by Western blot analysis. Reactive oxygen and nitrogen species (ROS/RNS) and superoxide dismutase (SOD) activity were determined by fluorometric and spectrometric methods, respectively. Results Although there was no embryo implantation in paraquat-treated mice, 5 out of 9 SRT1720+Paraquat-treated mice had implantation sites which were significantly higher compared to the paraquat-treated group. Sirtuin-1 and FoxO1 expressions were increased at implantation sites of SRT1720-treated mice. ROS/RNS levels were decreased, while deacetylated FoxO1 levels and SOD activity were increased in SRT1720-treated mice. Conclusion Our findings suggest that sirtuin-1 may play a role in embryo implantation against oxidative stress through FoxO1-SOD signaling.
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