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Open AccessArticle

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

Department of Physiology and Pathophysiology, Medical University of Varna, Varna 9002, Bulgaria
Department of Preclinical and Clinical Sciences, Medical University of Varna, Varna 9002, Bulgaria
Department of General and Clinical Pathology, Forensic Science and Deontology, Medical University of Varna, Varna 9010, Bulgaria
Department of Biochemistry, Molecular Medicine and Nutrigenomics, Medical University of Varna; Varna 9002, Bulgaria
Author to whom correspondence should be addressed.
Molecules 2018, 23(4), 749;
Received: 22 February 2018 / Revised: 20 March 2018 / Accepted: 21 March 2018 / Published: 24 March 2018
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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