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    Melatonin attenuates caspase-dependent apoptosis in the thoracic aorta by regulating element balance and oxidative stress in pinealectomised rats
    (Canadian Science Publishing, 2019) Doganlar, Zeynep Banu; Uzun, Metehan; Ovali, Mehmet Akif; Dogan, Ayten; Ongoren, Gulin; Doganlar, Oguzhan
    The aim of this study was to explain the possible mechanisms by which melatonin deficiency results in cardiovascular injury and to investigate the effects of melatonin administration on important signalling pathways and element equilibrium in the thoracic aorta (TA). For this purpose, we analysed the cellular and molecular effects of melatonin deficiency or administration on oxidative stress, DNA damage, molecular chaperone response, and apoptosis induction in TA tissues of pinealectomised rats using ELISA, RAPD, qRT-PCR, and Western blot assays. The results showed that melatonin deficiency led to an imbalance in essential element levels, unfolded or misfolded proteins, increased lipid peroxidation, and selectively induced caspasedependent apoptosis in TA tissues without significantly affecting the Bcl-2/BAX ratio (2.28 in pinealectomised rats, 2.73 in pinealectomised rats treated with melatonin). In pinealectomised rats, the genomic template stability (80.22%) was disrupted by the significantly increased oxidative stress, and heat shock protein 70 (20.96-fold), TNF-alpha (1.73-fold), caspase-8 (2.03-fold), and caspase-3 (2.87-fold) were markedly overexpressed compared with the sham group. Melatonin treatment was protective against apoptosis and inhibited oxidative damage. In addition, melatonin increased the survivin level and improved the regulation of element equilibrium in TA tissues. The results of the study indicate that melatonin deficiency induces TNF-alpha-related extrinsic apoptosis signals and that the administration of pharmacological doses of melatonin attenuates cardiovascular toxicity by regulating the increase in the rate of apoptosis caused by melatonin deficiency in TA tissue of Sprague-Dawley rats.
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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.
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    Potential Biomarkers for Melatonin Deficiency in Thoracic Aorta and Left Ventricle of Pinealectomised Rats
    (Wiley-Blackwell, 2015) Doganlar, Oguzhan; Uzun, Metehan; Doganlar, Zeynep Banu; Ovali, Mehmet Akif; Ongoren, Gulin
    [Abstract Not Available]
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    The Role of Melatonin in Oxidative Stress, DNA Damage, Apoptosis and Angiogenesis in Fetal Eye under Preeclampsia and Melatonin Deficiency Stress
    (Taylor & Francis Inc, 2019) Doganlar, Zeynep Banu; Guclu, Hande; Oztopuz, Ozlem; Turkon, Hakan; Dogan, Ayten; Uzun, Metehan; Doganlar, Oguzhan
    Aim: The aim of this study was to investigate the possible mechanisms of ocular damage induced by pinealectomy (PNX) and preeclampsia (PE), and to determine the cellular and molecular effects of melatonin treatment on oxidative stress, DNA damage, molecular chaperone responses, induction of apoptosis and angiogenesis in the fetal eye of both PNX and PNX+PE animals. Material and Methods: We analysed therapeutic potential of melatonin on fetal eye damage in PNX and PNX+PE animals using Malondialdehyde (MDA), Random Amplified Polymorphic DNA (RAPD), qRT-PCR and Western blot assays. Results: Our study presents three preliminary findings: (a) in fetal eye tissues, PNX and PNX+PE significantly induce oxidative damage to both DNA and protein contents, leading to a dramatic increase in caspase-dependent apoptotic signalling in both mitochondrial and death receptor pathways; (b) the same conditions trigger hypoxia biomarkers in addition to significant overexpression of HIF1-alpha, HIF1-beta, MMP9 and VEGF genes in the fetal eye; (c) finally, melatonin regulates not only the expression of genes encoding antioxidant enzymes and increase in DNA damage as well as lipid peroxidation but also limits programmed cell death processes in the fetal eye of PNX and PNX+PE animals . Furthermore, melatonin can relatively modulate genes in the HIF1 family, TNF-alpha and VEGF, thus acting as a direct anti-angiogenic molecule. In conclusion, both PNX and PNX+PE induce ocular damage at both cellular and molecular levels in fetal eye tissue of rats. Conclusion: Our results clearly indicate the potential of melatonin as a preventative therapeutic intervention for fetal ocular damage triggered by both PNX and PNX+PE.