Heme oxygenase-1 expression and oxidative  stress - related markers in gastric mucosa in skin burns and protection with melatonin

Hristova, Mariyana G.; Bekyarova, Ganka; Tzaneva, Maria

doi:10.15547/tjs.2016.04.001

Cited by 6 publications

(14 citation statements)

References 39 publications

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“…In addition, melatonin reduces the membrane cytotoxic activity of TNF-α [ 52 ] and overproduction of NO/iNOS/ONOO- as well as diminishes their deleterious effects on mitochondria [ 53 ]. Our data support these claims [ 39 ].…”

Section: Discussionsupporting

confidence: 91%

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

et al. 2018

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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.

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Section: Discussionsupporting

confidence: 91%

“…Data suggested that TNF-α induced apoptosis of enterochromaffin-like cells by activating NF kappa B and generating NO [ 37 , 38 ]. In addition, immunohistochemically, we found increased iNOS expression in the epithelial cell cytoplasm in burned rats [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2018

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“…iNOS is a key enzyme of "classically activated" or "killer" macrophages (M1) and contributes to NO synthesis from L-arginin (24). In support of these results in a previous study, we found increased expression of iNOS (25). Upregulated NO/iNOS production and its interaction with superoxide radicals leads to production of highly toxic peroxynitrite radical.…”

Section: Discussionsupporting

confidence: 90%

Apoptosis as a mechanism for burn-induced gastric mucosal injury

Hristova¹,

Tzaneva²,

Bekyarova³

et al. 2018

Scripta Scientifica Medica

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INTRODUCTION: Severe thermal burns disturb tissue homeostasis of many organs, but the exact mechanisms of gastric mucosa changes are not yet clear. Various cellular mechanisms, such as cell activation, mitochondrial dysfunction, free oxygen radicals and cytokine overproduction may be involved in this process. AIM: The aim of this study was to assess the levels of malondialdehyde (MDA), apoptotic proteins Bax and Bcl-2 in normal gastric mucosa and to test the hypothesis that oxidative stress activation induces apoptotic processes in the stomach after experimental thermal trauma. MATERIALS AND METHODS: Under anesthesia, the shaved rats' dorsum was exposed to 90° C bath for 10 s to induce third-degree burn injury, involving 30% of the total body surface area. We determined the tissue level of MDA, a lipid peroxidation marker, by spectrophotometric method and the apoptosis of epithelial cells in gastric mucosa, which was immunohistochemically determined at the level of Bcl-2 and Bax in burn trauma. RESULTS: The gastric MDA level was higher (p<0.01) in the burned group compared to the control group 24 hours after thermal injury. The gastric mucosa in the treated group showed congestion, degenerative changes in the surface epithelium, focal destruction of glandular epithelium with formation of acute erosions. Bax expressed moderately in epithelial cells, predominantly in the basal parts of the gastric glands, while in the control group protein content was localized in the same region, but it was weak. Bcl-2 protein in the control group revealed nuclear expression in surface epithelium, while in the basal layer of gastric mucosa the expression was moderate and mainly cytoplasmic. In the burned group, Bcl-2 expression was more diffuse, nuclear and cytoplasmic, but cytoplasmic expression was weak. CONCLUSION: Thermal skin trauma induces gastric mucosal injury through the activation of lipid peroxidation, increase of pro-apoptotic Bax protein expression and decrease of anti-apoptotic Bcl-2 protein expression in epithelial cells. We suggest that apoptosis is a possible mechanism for structural changes in the gastric mucosa.

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“…The possible mechanism is via overexpression of HO-1. The upregulated HO-1could suppressed NF-κB signaling pathway and pro-inflammatory cytokines induced iNOS expression (Hristova et al 2016;Yang et al 2017). Previous studies reported that H 2 S has enhanced the activity of endothelial nitric oxide synthase (eNOS) by facilitating phosphorylation of its active site and dephosphorylation of the inhibitory site to increase the production of anti-inflammatory NO.…”

Section: Immunohistochemical Assessment Of Inosmentioning

confidence: 99%

H2S attenuates acute lung inflammation induced by administration of lipopolysaccharide in adult male rats

Ali¹,

Abdel-Hamid²,

Toni³

2018

gpb

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. Hydrogen sulfide (H2S) is gasotransmitter which plays an important role in human physiology. In this study, we aimed to check the effect of H2S treatment on acute lung inflammation (ALI). Thirty-six adult male albino rats were used and divided into: control group, ALI group which was intraperitoneally (i.p.) injected with lipopolysaccharide (LPS) at a dose of 5 mg/kg body weight, ALI group treated by the H2S donor; sodium hydrosulfide (NaHS) at a dose of 10 mg/kg body weight i.p. and ALI group treated by i.p. injection of 80 mg/kg body weight DL- propargylglycine (PAG) which is an inhibitor of endogenous H2S synthesis. Serum was obtained to determine interleukin-6 (IL-6) levels. Lipid peroxides and total antioxidant capacity (TAC) levels were measured in lung. Lung histopathology and expression of inducible nitric oxide synthase (iNOS) were also done. Results showed that NaHS improved lung inflammation through its inhibitory effect on iNOS expression, decreasing the levels of IL-6 and lipid peroxides and increasing TAC levels. But, ALI was exacerbated with PAG administration. In conclusion, the results proved that H2S has a protective effect against LPS induced ALI due to its anti-nitrative, anti-oxidant and anti-inflammatory properties.

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Heme oxygenase-1 expression and oxidative stress - related markers in gastric mucosa in skin burns and protection with melatonin

Cited by 6 publications

References 39 publications

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

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

Apoptosis as a mechanism for burn-induced gastric mucosal injury

H2S attenuates acute lung inflammation induced by administration of lipopolysaccharide in adult male rats

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