Doganlar, OguzhanDoganlar, Zeynep BanuOvali, Mehmet AkifGuclu, OrkutDemir, UfukDogan, AytenUzun, Metehan2024-06-122024-06-1220201064-19551525-6065https://doi.org/10.1080/10641955.2020.1802595https://hdl.handle.net/20.500.14551/23291Objective 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.en10.1080/10641955.2020.1802595info:eu-repo/semantics/closedAccessPreeclampsiaHeartFetusApoptosisOxidative StressMelatoninReduced Uterine PerfusionExpressionHypoxiaHypertensionAntioxidantPregnancyPressureDiseaseLevelSerumMelatonin regulates oxidative stress and apoptosis in fetal hearts of pinealectomised RUPP ratsArticle394429443Q3WOS:0005595651000012-s2.0-8508944876232791955Q2