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Burn injury induces histopathological changes and cell proliferation in liver of rats

机译:烧伤导致大鼠肝脏组织病理学改变和细胞增殖

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摘要

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.
机译:目的:通过组织病理学和炎性标志物分析,研究重度烧伤对大鼠肝脏的影响。方法:将42只雄性Wistar大鼠分为对照组(C)和烫伤性BI(SBI)两组。假手术后第1、4和14天对动物实施安乐死,占全身体表BI的45%。肝碎片进行组织病理学,形态定量(肝细胞面积和细胞密度),ciclooxigenase-2(COX-2)免疫表达和基因表达[肿瘤坏死因子(TNF)-α的实时聚合酶链反应,诱导型一氧化氮合酶(iNOS)和caspase-3]方法。结果:组织病理学结果显示,在所有研究阶段均出现炎症过程,并且在损伤后14 d肝细胞变性增加了结缔组织的数量。与对照组相比,SBI组的肝细胞面积,双核肝细胞密度和正弦细胞密度增加。 SBI组的COX-2免疫表达较强。结论:BI诱导大鼠肝脏组织病理学改变,COX-2免疫表达上调和细胞增殖。

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