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Molecules 2018, 23(4), 749; https://doi.org/10.3390/molecules23040749

Molecular Mechanisms of Melatonin Protection from Gastric Mucosal Apoptotic Injury in Experimental Burns

1
Department of Physiology and Pathophysiology, Medical University of Varna, Varna 9002, Bulgaria
2
Department of Preclinical and Clinical Sciences, Medical University of Varna, Varna 9002, Bulgaria
3
Department of General and Clinical Pathology, Forensic Science and Deontology, Medical University of Varna, Varna 9010, Bulgaria
4
Department of Biochemistry, Molecular Medicine and Nutrigenomics, Medical University of Varna; Varna 9002, Bulgaria
*
Author to whom correspondence should be addressed.
Received: 22 February 2018 / Revised: 20 March 2018 / Accepted: 21 March 2018 / Published: 24 March 2018
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Abstract

Melatonin, a basic secretory pineal gland product, is a nontoxic, multifunctional molecule. It has antioxidant and anti-apoptotic activities and protects tissues from injury. The objective of the present study was to determine the molecular mechanism of melatonin anti-apoptotic effect on gastric injury in a rat burn model. We hypothesized that melatonin gastric protection may be related to the activation of transcription erythroid 2-related factor 2 (Nrf2). Using a 30% total body surface area (TBSA) rat burn model, melatonin (10 mg/kg, i.p.) was injected immediately and 12 h after thermal skin injury. Via light immunohistochemistry, we determined the tissue level of 4-hydroxy-2-nonenal (4-HNE) as a marker of lipid peroxidation, Bcl-2 and Bax as apoptosis-related proteins, and Nrf2. Results are presented as medians (interquartile range (IQR)). Thermal trauma in burned animals, compared with the controls, increased the expression of pro-apoptotic Bax protein (1.37 (0.94–1.47)), decreased anti-apoptotic Bcl-2 protein (1.16 (1.06–1.23), p < 0.001) in epithelial cells, and elevated Bax/Bcl-2 ratios (p < 0.05). Tissue 4-HNE and Nrf2 levels were increased following severe burns (1.55 (0.98–1.61) and 1.16 (1.01–1.25), p < 0.05, respectively). Melatonin significantly decreased 4-HNE (0.87 (0.74–0.96), p < 0.01) and upregulated Nrf2 (1.55 (1.52–1.65), p < 0.001) levels. It also augmented Bax (1.68 (1.5–1.8), p < 0.001) and Bcl-2 expressions (1.96 (1.89–2.01), p < 0.0001), but reduced Bax/Bcl-2 ratios (p < 0.05). Our results suggest that experimental thermal trauma induces oxidative gastric mucosal injury. Melatonin manifests a gastroprotective effect through Nrf2 activation, lipid peroxidation attenuation, and Bax/Bcl-2 ratio modification as well. View Full-Text
Keywords: melatonin; burns; gastric injury; 4-HNE, Bcl-2; Bax; Nrf2 melatonin; burns; gastric injury; 4-HNE, Bcl-2; Bax; Nrf2
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Hristova, M.; Tzaneva, M.; Bekyarova, G.; Chivchibashi, D.; Stefanova, N.; Kiselova-Kaneva, Y. Molecular Mechanisms of Melatonin Protection from Gastric Mucosal Apoptotic Injury in Experimental Burns. Molecules 2018, 23, 749.

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