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 ...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(i NOS) 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, i NOS and caspase-3 gene expression. CONCLUSION: BI induces histopathological changes, upregulation of COX-2 immunoexpression, and cell proliferation in liver of rats.展开更多
基金Sao Paulo Research Foundation,FAPESP,No.11/22034-9
文摘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(i NOS) 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, i NOS and caspase-3 gene expression. CONCLUSION: BI induces histopathological changes, upregulation of COX-2 immunoexpression, and cell proliferation in liver of rats.
