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    Melatonin Improves Left Ventricular Mitochondrial Dynamics in Rats
    (Pleiades Publishing Inc, 2022) Uzun, Metehan; Oztopuz, Ozlem; Eroglu, Huseyin Avni; Doganlar, Oguzhan; Doganlar, Zeynep Banu; Ovali, Mehmet Akif; Demir, Ufuk
    There is increasing awareness that efficient and regular mitochondrial dynamics improvement cardiac function and affects the quality of life. Melatonin is a main pineal gland hormones and ameliorates mitochondrial dynamics in many cardiac disorders. For that purpose, we administrated melatonin to healthy rats all day long in order to investigate change in left ventricle mitochondrial dynamics both in the end of the nighttime and daytime. Twenty male Wistar rats (3-4 months age) were randomly assigned into Control (C; n = 10) and Melatonin groups (MEL; 10 mg/kg melatonin added drinking water, n = 10). On the 5th day of the study, 5 rats from the groups were randomly selected and euthanized at 08:00 AM and the remaining 5 rats were euthanized at 20:00 PM from each groups and samples of left ventricle (LV) tissue were harvested. Quantitative real-time PCR and western blot analysis demonstrated that melatonin acts preventive role on mitochondrial fusion and mitophagy through the DRP1/FIS1 and BNIP3/NIX axis, respectively. Additionally, melatonin administration significantly reduced P21 activation, induced cell cycle arrest, P27, finally regulated caspase-depended mitochondrial apoptosis signals in a time dependent manner. Our results suggest that melatonin may emerge as a therapeutic candidate to protect the bioenergetic dynamics of mitochondria in hearth.
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    Melatonin regulates oxidative stress and apoptosis in fetal hearts of pinealectomised RUPP rats
    (Taylor & Francis Inc, 2020) Doganlar, Oguzhan; Doganlar, Zeynep Banu; Ovali, Mehmet Akif; Guclu, Orkut; Demir, Ufuk; Dogan, Ayten; Uzun, Metehan
    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.