Basic Study
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Feb 28, 2016; 8(6): 322-330
Published online Feb 28, 2016. doi: 10.4254/wjh.v8.i6.322
Burn injury induces histopathological changes and cell proliferation in liver of rats
Jeferson André Bortolin, Hananiah Tardivo Quintana, Tabata de Carvalho Tomé, Flavia Andressa Pidone Ribeiro, Daniel Araki Ribeiro, Flavia de Oliveira
Jeferson André Bortolin, Hananiah Tardivo Quintana, Tabata de Carvalho Tomé, Flavia Andressa Pidone Ribeiro, Daniel Araki Ribeiro, Flavia de Oliveira, Department of Biosciences, Federal University of São Paulo (UNIFESP), Santos, SP 11060-001, Brazil
Author contributions: Bortolin JA performed the majority of experiments and analyzed the data; Quintana HT and Tomé TC participated in treatment of animals; Ribeiro FAP performed the molecular investigation; Ribeiro DA wrote the paper; de Oliveira F wrote the paper, designed and coordinated the research; all authors critically reviewed the manuscript and approved it.
Supported by São Paulo Research Foundation, FAPESP, No. 11/22034-9.
Institutional review board statement: None.
Institutional animal care and use committee statement: Committee of Ethics and Research from Federal University of São Paulo (protocol number 329/12).
Conflict-of-interest statement: The authors do not disclose any conflicts of interest.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Flavia de Oliveira, PhD, Department of Biosciences, Federal University of São Paulo (UNIFESP), Rua Silva Jardim, 136 - Lab 328, Vila Mathias CEP, Santos, SP 11060-001, Brazil. flavia.oliveira@unifesp.br
Telephone: +55-13-38783844
Received: June 27, 2015
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
Abstract

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.

Keywords: Burn injury, Morphology, Histophatology, Liver, Ciclooxigenase-2

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.