Protective effects of insulin treatment in the morphological alterations and oxidative damage to DNA in the liver of young rats subjected to skin scald burn injury.

Background: Burn injury (BI) represents a major epidemiologic problem worldwide, mostly in children. BIs greater than 40% of the total body surface, are considered severe, and entail a hepatic hypermetabolic response, which is associated with proteins depletions and prolonged hypermetabolism.

Objective: This study aims to evaluated the effects of short- and long-term insulin treatment on liver morphology and the use of a biomarker related to oxidative damage to DNA (8-OHdG) to better understand the anabolic action of this hormone in the liver.

Methods: Wistar rats aged 21 d were distributed into four groups: control (C), control with insulin (C+I), scald burn injury (SBI), and SBI with insulin (SBI+I). The SBI groups were subjected to a burn 45% total body surface area. The C+I and SBI+I groups received insulin (5 UI/Kg/d) for 4- or 14 d. The livers were analyzed for morphometric, histopathological, and immunohistochemical for 8-OHdG.

Results: The main results showed that, in a short time, insulin increases the density of binucleated hepatocytes as an organ response to burn injury. In the long term, insulin increased the area of hepatocytes in the SBI+I group in relation to SBI, highlighting the similar values between the SBI+I and the control groups. Regarding sinusoidal cells, insulin was able to modulate this liver proliferative reaction. Insulin reduces 8-OHdG immunoexpression in short and long-term post-burn moments.

Conclusion: The insulin modulation of 8-OHdG makes us infer that a study about the control of 8-OHdG as a potential biomarker in patients could be an efficient precursor of the level of oxidative stress associated with hepatic dysfunction associated to extensive burn injury.