Published online Feb 28, 2016. doi: 10.4254/wjh.v8.i6.322
Peer-review started: June 30, 2015
First decision: October 6, 2015
Revised: January 7, 2016
Accepted: January 21, 2016
Article in press: January 22, 2016
Published online: February 28, 2016
AIM: To investigate effects of severe burn injury (BI) in rat liver through the histopathological and inflammatory markers analysis.
METHODS: Forty-two male Wistar rats were distributed into two groups, control (C) and subjected to scald BI (SBI). The animals were euthanized one, four and 14 d post sham or 45% of the total body surface BI. Liver fragments were submitted to histopathological, morphoquantitative (hepatocyte area and cell density), ciclooxigenase-2 (COX-2) immunoexpression, and gene expression [real-time polymerase chain reaction for tumor necrosis factor (TNF)-α, inducible nitric oxide synthase (iNOS) and caspase-3] methods.
RESULTS: Histopathological findings showed inflammatory process in all periods investigated and hepatocyte degeneration added to increased amount of connective tissue 14 d post injury. Hepatocyte area, the density of binucleated hepatocytes and density of sinusoidal cells of SBI groups were increased when compared with control. COX-2 immunoexpression was stronger in SBI groups. No differences were found in TNF-α, iNOS and caspase-3 gene expression.
CONCLUSION: BI induces histopathological changes, upregulation of COX-2 immunoexpression, and cell proliferation in liver of rats.
Core tip: Severe burn injuries result in serious complications that involve host response related to inflammation and multiple organ dysfunction. The goal of this study was to investigate the temporal effects of extensive experimental burn injury (BI) in rat liver through the histopathological and morphoquantitative aspects, immunoexpression of ciclooxigenase-2 (COX-2) and liver gene expression of tumor necrosis factor-α, inducible nitric oxide synthase and caspase-3. Our results revealed that BI induces histopathological changes, upregulation of COX-2 immunoexpression, and cell proliferation in liver of rats.