Trauma increases extrahepatic arginase activity
Trauma increases extrahepatic arginase activity
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DOI：
10.1067/msy.2000.104745
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发表时间：
2000-04-01
期刊：
影响因子：
3.8
通讯作者：
Kearney, PA
中科院分区：
文献类型：
--
作者：
Ochoa, JB;Bernard, AC;Kearney, PA
背景。虽然主要以五英镑表示；精氨酸酶活性也存在于肝外组织中，特别是巨噬细胞中，它可能在伤口愈合、细胞增殖和一氧化氮产生的调节中发挥多种生理作用。免疫细胞中的精氨酸酶活性会被某些细胞因子（例如 IL-4、IL-10 和 TGF-β）以及儿茶酚胺上调。由于创伤后这些物质的释放增加，我们假设创伤后免疫细胞中的精氨酸酶活性也会增加。目前的工作检验了这一假设。方法。通过进行剖腹探查术在 C3H/HeN 小鼠中创建手术创伤模型。测定组织精氨酸酶活性和精氨酸酶 I 蛋白表达。作为对照，精氨酸酶活性和表达也通过使用内毒素而受到刺激。此外，我们还评估了诱导型一氧化氮合酶的表达和血浆中一氧化氮代谢物的积累。结果。手术创伤与脾和肾组织中精氨酸酶活性显着增加相关（P < .05）。来自创伤动物的脾巨噬细胞的精氨酸酶活性水平约为对照组的 10 倍 (P < .05)。单独的内毒素增加了脾脏中的精氨酸酶活性，但这种增加小于单独的创伤（P < .05）。精氨酸酶活性在创伤后持续升高长达 4 天，并在第 7 天恢复正常。脾和肾组织中的精氨酸酶 I 表达均因创伤和仅脾脏中的内毒素而上调。尽管创伤动物中诱导型一氧化氮合酶上调，但与对照组相比，创伤后 2 天循环一氧化氮代谢物减少 (P < .05)。与单独进行内毒素治疗相比，内毒素诱导的一氧化氮代谢物在创伤动物中也有所减少 (P < .05)，但这在第 4 天时恢复正常。结论。创伤后肝外精氨酸酶表达和活性增加，可能为细胞增殖和修复提供必要的前体，或者可能在一氧化氮的产生中发挥调节作用。
Background. Although expressed primarily in the fiver; arginase activity also is present in extrahepatic tissues and specifically in macrophages, where it may play diverse physiologic roles in wound healing, cellular proliferation, and the regulation of nitric oxide production. Arginase activity in immune cells is upregulated by certain cytokines such as IL-4, IL-10, and TGF-beta and by catecholamines. Since the release of these substances is increased after trauma, we hypothesized that arginase activity would also be increased in immune cells after trauma. The current work tests this hypothesis.Methods. A model of surgical trauma was created in C3H/HeN mice by performing an exploratory laparotomy. Tissue arginase activity and arginase I protein expression were determined. As a control, arginase activity and expression were also stimulated-with the use of endotoxin. In addition, we evaluated the expression of inducible nitric oxide synthase and the accumulation of nitric oxide metabolites in plasma.Results. Surgical trauma was associated with a significant increase in arginase activity in splenic and renal tissues (P < .05). Splenic macrophages from trauma animals exhibited arginase activity levels approximately 10 times those of controls (P < .05). Endotoxin alone increased arginase activity in the spleen, but this increase was less than that of trauma alone (P < .05). Arginase activity remained elevated after trauma for up to 4 days and normalized by day 7. Arginase I expression was upregulated by trauma in both splenic and renal tissue and by endotoxin in the spleen only. Despite upregulation of inducible nitric oxide synthase in trauma animals, circulating nitric oxide metabolites were decreased 2 days after trauma compared with controls (P < .05). Endotoxin-induced nitric oxide metabolites were also reduced in trauma animals compared with endotoxin treatment alone (P < .05), but this normalized by day 4.Conclusions. Extrahepatic arginase expression and activity is increased after trauma and may provide the necessary precursors for cellular proliferation and repair or may play a regulatory role in the production of nitric oxide.