Melatonin attenuates caspase-dependent apoptosis in the thoracic aorta by regulating element balance and oxidative stress in pinealectomised rats

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dc.authoriduzun, metehan/0000-0003-1406-5473
dc.authoridDoganlar, Oguzhan/0000-0003-2654-7269
dc.contributor.authorDoganlar, Zeynep Banu
dc.contributor.authorUzun, Metehan
dc.contributor.authorOvali, Mehmet Akif
dc.contributor.authorDogan, Ayten
dc.contributor.authorOngoren, Gulin
dc.contributor.authorDoganlar, Oguzhan
dc.date.accessioned2025-01-27T20:26:51Z
dc.date.available2025-01-27T20:26:51Z
dc.date.issued2019
dc.departmentÇanakkale Onsekiz Mart Üniversitesi
dc.description.abstractThe 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.
dc.description.sponsorshipTrakya University Scientific Research Fund [TUBAP 2015/45]
dc.description.sponsorshipThis study was supported by the Trakya University Scientific Research Fund (TUBAP 2015/45).
dc.identifier.doi10.1139/apnm-2018-0205
dc.identifier.endpage163
dc.identifier.issn1715-5312
dc.identifier.issn1715-5320
dc.identifier.issue2
dc.identifier.pmid30058356
dc.identifier.scopus2-s2.0-85060651533
dc.identifier.scopusqualityQ2
dc.identifier.startpage153
dc.identifier.urihttps://doi.org/10.1139/apnm-2018-0205
dc.identifier.urihttps://hdl.handle.net/20.500.12428/22464
dc.identifier.volume44
dc.identifier.wosWOS:000456999200007
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherCanadian Science Publishing
dc.relation.ispartofApplied Physiology Nutrition and Metabolism
dc.relation.publicationcategoryinfo:eu-repo/semantics/openAccess
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20250125
dc.subjectoxidative stress
dc.subjectintrinsic and extrinsic apoptosis signalling
dc.subjectcaspases
dc.subjectmelatonin
dc.titleMelatonin attenuates caspase-dependent apoptosis in the thoracic aorta by regulating element balance and oxidative stress in pinealectomised rats
dc.typeArticle

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