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.