Abstract
Melatonin, the principal secretory product of the pineal gland, functions as a potent antioxidant and free radical scavenger. Additionally, the antiapoptotic effect of melatonin has been observed both in vivo and in vitro. The aim of this study was to investigate the protective effects of melatonin against burn-induced injury in rat liver and whether these changes were associated with oxidative stress and changes in the expression of apoptosis related genes Bcl-2 and Bax. Melatonin (10 mg/kg, i.p.) was applied immediately after 30% of total body surface area (TBSA) burns of male Wistar rats. Malondialdehyde (MDA) as marker of oxidative stress and tumor necrosis factor (TNF-α) as inflammatory marker were assayed by biochemical methods. The hepatic apoptosis related genes Bcl-2 and Bax using light immunоchistochemistry were investigated, too. Hepatic TNF-α and MDA levels were increased significantly following severe burn. Thermal trauma increased the Bax expression without any changes of anti-apoptotic Bcl-2 protein in sinusoidal endothelial cells (SECs) of burn-treated animals compared with the control group animals as well as elevated ratio Bax/Bcl-2 suggesting the susceptibility of these cells to apoptosis. Melatonin significantly decreased the MDA and TNF-α levels in the liver tissue. It decreased also expression of Bax, increased expression of Bcl-2 and reduced Bax/Bcl-2 ratio. In conclusion, experimental data show that melatonin modulates the expression of Bcl-2 family proteins by increasing anti-apoptotic Bcl-2, inhibits apoptosis and restricts the burn-induced damage.
Highlights
Severe burn is still a serious clinical problem in emergency medicine causing damages to organs distant from burn wound
When the rats were treated with melatonin, the concentration of hepatic tumor necrosis factor (TNF)-α decreased by 21% significantly, reaching the control values at the 24th hour after burns (Figure 2). 3.2
Changes in the Expression on Apoptosis-Related Bcl-2 in Liver The expression of Bcl-2 was detected in sinusoidal endothelial cells (SECs) in the control group (Figure 3)
Summary
Severe burn is still a serious clinical problem in emergency medicine causing damages to organs distant from burn wound. Various cellular and molecular interactions such as neutrophil and macrophage activation, mitochondrial dysfunction oxygen radical, cytokine overproduction, depletion of glutathione, may be involved in the processes [3,4,5,6]. These complex mechanisms cause liver dysfunction, alteration of hepatic parenchyma and eventually cell death (apoptosis). The increased apoptosis in liver and other organs is a result of “systemic apoptotic response” after burns [7]. The increased ROS production results in an imbalance between anti-apoptotic Bcl-2 and pro-apoptotic Bax proteins which contributes to the susceptibility of the cell to apoptosis. Literature data about the role of free radicals in liver apoptosis after burns are scarce
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