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首页> 外文期刊>Shock: Molecular, cellular, and systemic pathobiological aspects and therapeutic approaches = The official journal of the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies >Role of reactive oxygen species for hepatocellular injury and heme oxygenase-1 gene expression after hemorrhage and resuscitation.
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Role of reactive oxygen species for hepatocellular injury and heme oxygenase-1 gene expression after hemorrhage and resuscitation.

机译：肝细胞活性氧的作用损伤和血红素oxygenase-1基因表达出血和复苏。

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摘要

Reactive oxygen species (ROS) generated during hemorrhage and subsequent resuscitation (H/R) may contribute to cellular injury but may also regulate an adaptive cellular response to stress. Heme oxygenase (HO)-1 has been recognized as an important stress-inducible gene conferring protection after H/R. The aim of this study was to determine the contribution of ROS to hepatocellular injury and to induction of HO-1 in parenchymal and nonparenchymal cells after H/R. Anesthetized Sprague-Dawley rats were subjected to reversible H/R with or without coadministration of the potent antioxidant Trolox (6 mg/kg body wt). HO-1 gene expression was determined at baseline, at the end of hemorrhagic hypotension, and after 1, 3, and 5 h of resuscitation on the messenger ribonucleic acid (mRNA) and protein level. Assessment of hepatocellular injury by alpha-glutathione-S-transferase serum levels showed a significant increase after H/R that was attenuated by Trolox (sham: 38 (26-42); H/R: 286 (150-696); Trolox: 14 (2-227) microg/L; median (25th/75th percentile) P<0.05). Injury correlated with induction of HO-1 mRNA (r2 = 0.97) on the whole organ level and with the expression pattern of HO-1-immunoreactive protein in pericentral hepatocytes after H/R. Trolox attenuated H/R-induced increase of HO-1 in hepatocytes. In contrast, nonparenchymal cells showed high constitutive levels of HO-1 mRNA and protein that were increased by sham operation and H/R to a similar extent. HO-1 steady-state transcripts in nonparenchymal cells were not modulated by Trolox. These results suggest a differential regulation of HO-1 gene expression in hepatocytes and nonparenchymal cells. ROS formation seems to contribute to early hepatocellular injury but also serves as an important trigger for HO-1 gene expression in parenchymal cells, which confers delayed protection after H/R.
机译：活性氧(ROS)生成的期间出血和随后的复苏(H / R)导致细胞损伤,但也可能调节压力的适应性细胞反应。血红素加氧酶(HO) 1被公认为一个重要stress-inducible基因赋予保护后H / R。确定ROS的贡献肝细胞损伤和HO-1的感应实质和nonparenchymal细胞后H / R。麻醉Sprague-Dawley老鼠受到与或不可逆的H / R共同的强有力的抗氧化剂Trolox(6毫克/公斤的身体wt)。决定在基线,在出血性的结束低血压,后1、3和5 h复苏的信使核糖核酸(信使rna)和蛋白质水平。肝细胞损伤,alpha-glutathione-S-transferase血清水平显示H / R,后显著增加减毒Trolox(骗局:38 (26-42);(150 - 696);(25日/第75个百分位)P < 0.05)。与感应HO-1 mRNA (r2 = 0.97)整个器官水平和表达模式在中心周围的HO-1-immunoreactive蛋白质肝细胞后H / R。在肝细胞H / HO-1 R-induced增加。相反,nonparenchymal细胞显示高本构HO-1信使rna和蛋白质的水平是增加了虚假的操作和H / R类似的程度。nonparenchymal细胞没有调制Trolox。在肝细胞HO-1调节基因表达和nonparenchymal细胞。有助于早期肝细胞损伤也作为一个重要的触发HO-1基因薄壁组织的细胞中表达,授予延迟保护后H / R。

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