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

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  • معلومة اضافية
    • المصدر:
      Publisher: Canadian Science Publishing Country of Publication: Canada NLM ID: 101264333 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1715-5320 (Electronic) Linking ISSN: 17155312 NLM ISO Abbreviation: Appl Physiol Nutr Metab Subsets: MEDLINE
    • بيانات النشر:
      Publication: 2011- : Ottawa, ON : Canadian Science Publishing
      Original Publication: Ottawa, ON : National Research Council of Canada, c2006-
    • الموضوع:
      Aorta, Thoracic/*drug effects ; Apoptosis/*drug effects ; Caspases/*physiology ; Melatonin/*deficiency ; Melatonin/*pharmacology ; Oxidative Stress/*drug effects ; Pineal Gland/*physiology ; Water-Electrolyte Balance/*drug effects; Animals ; Aorta, Thoracic/physiology ; Genomics ; HSP70 Heat-Shock Proteins/metabolism ; Lipid Peroxidation/drug effects ; Male ; Proteostasis Deficiencies ; Rats ; Rats, Sprague-Dawley
    • نبذة مختصرة :
      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 caspase-dependent 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-α (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-α-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.
    • Contributed Indexing:
      Keywords: caspases; intrinsic and extrinsic apoptosis signalling; melatonin; mélatonine; oxidative stress; signalisation intrinsèque et extrinsèque de l’apoptose; stress oxydatif
    • الرقم المعرف:
      0 (HSP70 Heat-Shock Proteins)
      EC 3.4.22.- (Caspases)
      JL5DK93RCL (Melatonin)
    • الموضوع:
      Date Created: 20180731 Date Completed: 20191227 Latest Revision: 20191227
    • الموضوع:
      20231215
    • الرقم المعرف:
      10.1139/apnm-2018-0205
    • الرقم المعرف:
      30058356