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The mRNA expression patterns of tumor necrosis factor-ex and TNFR-I in some vital organs after thermal injury

机译:热损伤后一些重要器官中肿瘤坏死因子-ex和TNFR-1的mRNA表达模式

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AIM: To investigate changes of tumor necrosis factor-α (TNF-α) and TNFR-I expression in vital organs and their significance in the pathogenesis of multiple organ damage associated with endogenous endotoxin following major burns. METHODS: Wistar rats subjected to a 35 % full-thickness scald injury were sacrificed at 12 h, 24 h, 48 h, and 72 h postburn, respectively. Meanwhile, eight rats were taken as normal controls. Tissue samples from liver, spleen, kidney, lung and intestine were collected to assay tissue endotoxin levels and measure TNF-α and TNFR-I expression. In addition, blood samples were obtained for the determination of organ function parameters. RESULTS: Endotoxin levels in liver, spleen and lung increased markedly after thermal injury, with the highest level in liver. The gene expression of TNF-α in liver, lung and kidney was up-regulated after thermal injury, while the TNFR-I mRNA expression in liver, lung, kidney and intestine was shown decreased throughout the observation period. Thus, the mRNA expression ratio of TNF-α to TNFR-I was significantly increased postburn, particularly in pulmonary tissue (67-fold). In addition, the significant correlations between the expression of TNFR-I or the expression ratio of TNF-α/TNFR mRNA in liver tissue and serum aspartate aminotransferase levels were noted (P <0.05-0.01). Similar results were also obtained between pulmonary TNF-α mRNA expression and myeloperoxidase activities (P<0.01), whereas there was a highly negative correlation between levels of renal TNFR-I mRNA expression and serum creatinine. CONCLUSION: Burn injury could result in the translocation of gut-derived endotoxin that was mainly distributed in the liver, spleen and lung. The translocated endotoxin then made the expression of TNF-α and TNFR-I mRNA up-regulated and down-regulated respectively in various organs, which might be involved in the pathogenesis of multiple organ damage following burns.
机译:目的:探讨肿瘤坏死因子-α(TNF-α)和肿瘤坏死因子-I(TNFR-I)在重要器官中的表达变化及其在严重烧伤后与内源性内毒素相关的多器官损伤的发病机制中的意义。方法:Wistar大鼠在烧伤后12 h,24 h,48 h和72 h分别处死35%的全层烫伤。同时,将八只大鼠作为正常对照。收集来自肝,脾,肾,肺和肠的组织样品以测定组织内毒素水平并测量TNF-α和TNFR-1表达。另外,获得血液样品以确定器官功能参数。结果:热损伤后肝,脾,肺中内毒素水平明显升高,肝脏中内毒素水平最高。在热损伤后,肝,肺和肾中TNF-α的基因表达上调,而在整个观察期内,肝,肺,肾和肠中的TNFR-1 mRNA表达下降。因此,烧伤后TNF-α与TNFR-1的mRNA表达比率显着增加,特别是在肺组织中(67倍)。另外,肝组织中TNFR-1的表达或TNF-α/ TNFR mRNA的表达比例与血清天冬氨酸转氨酶水平之间存在显着相关性(P <0.05-0.01)。在肺TNF-αmRNA表达与髓过氧化物酶活性之间也获得了相似的结果(P <0.01),而肾TNFR-1 mRNA表达水平与血清​​肌酐之间存在高度负相关。结论:烧伤可导致肠源性内毒素易位,主要分布于肝,脾和肺。易位的内毒素随后使各种器官中的TNF-α和TNFR-1 mRNA的表达分别上调和下调,这可能与烧伤后多器官损伤的发病机理有关。

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