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Melatonin protection against burn-induced liver injury. A review

100%
Bekyarova G., Tzaneva M., Hristova M., Hristov K.
Open Medicine
|
2014
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vol. 9
|
issue 1
148-158
EN
Severe thermal injury may be complicated by dysfunction of organs distant from the original burn wound, including the liver, and represents a serious clinical problem. Although pathophysiology of burn-induced liver injury remains unclear, increasing evidence implicate activation of inflammatory response, oxidative stress, endothelial dysfunction and microcirculatory disorders as the main mechanisms of hepatic injury. Several studies suggest melatonin as a multifunctional indolamine that counteracts some of the pathophysiologic steps and displays significant beneficial effects against burn-induced cellular injury. This review summarizes the role of melatonin in restricting the burn-induced hepatic injury and focuses on its effects on oxidative stress, inflammatory response, endothelial dysfunction and microcirculatory disorders as well as on signaling pathways such as regulation of nuclear erythroid 2-related factor 2 (Nrf2) and nuclear factor-kappaB (NF-kB). Further studies are necessary to elucidate the modulating effect of melatonin on the transcription factor responsible for the regulation of the pro-inflammatory and antioxidant genes involved in burn injuries.
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Effective melatonin protection of burn-induced hepatic disorders in rats

84%
Bekyarova G., Bratchkova Y., Tancheva S., Hristova M.
Open Medicine
|
2012
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vol. 7
|
issue 4
533-538
EN
We studied the effect of melatonin on morphological and functional disorders using serum markers of liver dysfunction such as cholinesterase and gamma glutamyl transpeptidase, hepatic protein content and malondialdehyde in a burned-rat model. Melatonin (10 mg/kg (−1), i.p) was administered immediately and then 12 h after 30% of total body surface area burns of male Wistar rats. The burns induced an increase of hepatic malondialdehyde levels by 166% (p<0.001), and also vascular congestion, leukocyte infiltration around the central veins, intracellular vacuolization, hepatic cell degeneration and apoptotic bodies (Councilman’s bodies). These changes were associated with significantly reduced serum cholinesterase (36%), gamma glutamyl transpeptidase (76%), hepatic proteins (52%) and serum albumin (37%) (p<0.001–0.0001). Treatment with melatonin reduced elevated hepatic malondialdehyde values by 50% (p<0.01). Melatonin restricted degenerative alteration in the hepatocytes: it protected the burninduced decrease of serum gamma glutamyl transpeptidase activity by 48% (p<0.01), hepatic proteins by 64% (p<0.01), and serum activity of cholinesterase as the only marker of liver damaged synthetic function by 57% (p<0.0001) but did not exert any significant influence on serum albumin concentration. Melatonin repaired the pathomorphological lesions and functional disorders. It could restore liver damage following thermal injury in humans.
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