A protective role of interleukin 11 on hepatic injury in acute endotoxemia
A protective role of interleukin 11 on hepatic injury in acute endotoxemia
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DOI：
10.1097/01.shk.0000103386.98235.f6
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发表时间：
2004-02-01
期刊：
影响因子：
3.1
通讯作者：
Sassa, S
中科院分区：
文献类型：
--
作者：
Maeshima, K;Takahashi, T;Sassa, S
肝脏是脓毒症的主要靶器官之一，肝功能衰竭往往导致严重后果。有报道称，重组人白介素11(rhIL-11)是一种多效性细胞因子，可用于脓毒症的治疗。然而，IL-11在脓毒症患者肝功能衰竭中的作用尚未得到评估。在本研究中，我们观察了重组人白介素11对内毒素血症大鼠肝损伤的影响。雄性SD大鼠腹腔注射(Ip)诱发急性内毒素血症。细菌脂多糖(嘴唇，20毫克/公斤)。注射双唇后立即给予重组人白介素11(150 mg/kg，ip)。或者这辆车。LIPS治疗组大鼠血清丙氨酸氨基转移酶(ALT)和天冬氨酸转氨酶(AST)活性、肝细胞广泛坏死、肿瘤坏死因子-α(TNF-α)、诱导型一氧化氮合酶(INOS)和核因子-kappaB(NF-kappaB)DNA结合活性均显著升高。相反，rh IL-11治疗可显著改善内毒素所致的肝损伤，所有指标均有明显改善。此外，重组人IL-11治疗可显著降低内毒素诱导的死亡率。提示重组人IL-11对内毒素血症所致的肝损伤有明显的保护作用。
The liver is one of the major target organs affected in sepsis, and its failure always results in critical consequences. It has been reported that recombinant human interleukin 11 (rhIL-11), a pleiotropic cytokine, may be useful in the treatment of sepsis. However, the effect of IL-11 specifically on the hepatic failure in sepsis has not been evaluated. In the present study, we examined the effect of rhIL-11 on the hepatic injury in a rat endotoxemia model. Acute endotoxemia was induced in male Sprague-Dawley rats by intraperitoneal injection (i.p.) of bacterial lipopolysaccharide (LIPS, 20 mg/kg). Immediately after injection of LIPS, rats were treated with rhIL-11 (150 mug/kg, i.p.) or the vehicle. LIPS treatment induced severe hepatic injury as revealed by marked increases in serum alanine transaminase (ALT) and aspartate transaminase (AST) activities, extensive hepatocyte necrosis, tumor necrosis factor-alpha (TNF-alpha) mRNA, inducible nitric oxide synthase (iNOS) mRNA, and DNA-binding activity of nuclear factor-kappaB (NF-kappaB). In contrast, rhIL-11 treatment significantly ameliorated the LPS-incluced hepatic injury, as judged by marked improvement in all these indices. In addition, rhIL-11 treatment markedly decreased LPS-induced mortality. These results indicate that rhIL-11 plays a significant protective role in LPS-induced hepatic injury in acute endotoxemia.