Melatonin regulates oxidative stress and apoptosis in fetal hearts of pinealectomised RUPP rats

ABSTRACT

Objective: This study aimed to investigate the effects of melatonin on cardiac oxidative stress and apoptosis in the fetal heart in RUPP rats.

Methods: The fetal heart samples were obtained from melatonin administrated RUPP rats

Results: Our results indicate that preeclampsia exacerbated by melatonin deficiency triggers hypoxic conditions, both mis/un-folded protein response, oxidative stress-induced DNA damage and apoptosis. Melatonin treatment provided significant therapeutic effects on fetal hearts via regulating all these stress response at cellular and molecular levels.

Conclusion: Melatonin may be considered as a potential molecule for development of preventive strategies to reduce the PE induced risk of cardiovascular diseases in offspring.

KEYWORDS:

• Preeclampsia
• heart
• fetus
• apoptosis
• oxidative stress
• melatonin

Study limitations

We did not identify the sex of the fetuses nor did we determine the level of melatonin in the blood of the mother rats used in this study.

Notes of contributors

MU conducted the study, participated in the data collection and evaluation, and performed the animal experiments. MAO and UD helped to perform animal experiments and tissue harvesting. OD, ZBD, OG performed the laboratory analyses and the evaluation of the genetic parameters. AD worked as a technical assistant in the laboratory studies. OD performed the statistical analysis. MU and OD wrote the manuscript. All authors read and approved the final manuscript.

Disclosure statement

The authors declare that there is no conflict of interest.

Supplementary material

Supplemental data for this article can be accessed here.