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首页> 外文期刊>American Journal of Physiology >Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation.
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Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation.

机译：脂多糖结合蛋白可调节失血性休克和复苏后的肝损伤和炎症反应。

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Hemorrhagic shock and resuscitation cause endotoxemia and hepatocellular damage. Because lipopolysaccharide-binding protein (LBP) enhances cellular responses to endotoxin, our aim was to determine whether LBP contributes to hemorrhage/resuscitation-induced injury by comparing LBP knockout and wild-type mice. Under pentobarbital anaesthesia, wild-type and LBP-deficient mice were hemorrhaged to 30 mmHg for 3 h and then resuscitated with shed blood plus half the volume of lactated Ringer solution. Serum alanine aminotransferase (ALT) necrosis, neutrophil infiltration, and 4-hydroxynonenal by histology/cytochemistry and stress kinase activation by immunoblot analysis were then determined. ALT in wild-type mice was 2,461 +/- 383 and 1,418 +/- 194 IU/l (means +/- SE), respectively, at 2 and 6 h after resuscitation versus sham ALT of 102 +/- 6 IU/l. In LBP-deficient mice, ALT was blunted at both time points to 1,108 +/- 340 and 619 +/- 171 IU/l (P < 0.05). Liver necrosis after 6 h was also attenuated from 3.5+/- 0.8% in wild-type mice to 1.3 +/- 0.5% in LBP-deficient mice (P < 0.05). After hemorrhage/resuscitation, neutrophil infiltration increased 71% more in wild-type than LBP knockout mice. Similarly, hepatic 4-hydroxynonenal staining, indicative of lipid peroxidation, decreased from 33.8 +/- 4.5% in wild-type mice to 11.6 +/- 1.9% in knockout mice (P < 0.05). After hemorrhage/resuscitation, activation of MAPKs, JNK and ERK, occurred in wild-type mice, which was largely blocked in LBP-deficient mice. However, endotoxin in portal blood after resuscitation was not significantly different between wild-type and knockout mice. In conclusion, hemorrhagic shock and resuscitation to mice cause severe, LBP-mediated hepatocellular damage. An absence of LBP blunts hepatocellular injury with decreased neutrophil infiltration, oxidative stress, and c-Jun and ERK activation.
机译：失血性休克和复苏引起内毒素血症和肝细胞损伤。因为脂多糖结合蛋白（LBP）增强了细胞对内毒素的反应，所以我们的目的是通过比较LBP基因敲除小鼠和野生型小鼠来确定LBP是否有助于出血/复苏所致的损伤。在戊巴比妥麻醉下，将野生型和LBP缺陷型小鼠出血至30 mmHg，持续3 h，然后用流血加一半乳酸林格液复苏。然后通过组织学/细胞化学测定血清丙氨酸氨基转移酶（ALT）坏死，中性粒细胞浸润和4-羟基壬烯醛，并通过免疫印迹分析确定应激激酶活化。复苏后第2和第6小时，野生型小鼠的ALT分别为2,461 +/- 383和1,418 +/- 194 IU / l（平均+/- SE），而假手术ALT为102 +/- 6 IU / l 。在LBP缺陷小鼠中，ALT在两个时间点均变钝，分别为1,108 +/- 340和619 +/- 171 IU / l（P <0.05）。 6小时后的肝坏死也从野生型小鼠的3.5 +/- 0.8％减至LBP缺陷型小鼠的1.3 +/- 0.5％（P <0.05）。出血/复苏后，野生型中性粒细胞浸润比LBP敲除小鼠增加71％。同样，表示脂质过氧化的肝4-羟基壬烯染色从野生型小鼠的33.8 +/- 4.5％降至敲除小鼠的11.6 +/- 1.9％（P <0.05）。出血/复苏后，野生型小鼠发生了MAPKs，JNK和ERK的激活，而在LBP缺陷型小鼠中大部分被阻断。但是，野生型和基因敲除小鼠复苏后门静脉血中的内毒素没有显着差异。总之，对小鼠的失血性休克和复苏会导致严重的，LBP介导的肝细胞损伤。 LBP的缺乏使中性粒细胞浸润，氧化应激以及c-Jun和ERK活化减少而使肝细胞损伤变钝。

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