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首页> 外文期刊>Cytokine >IL-6 Promotes compensatory liver regeneration in cirrhotic rat after partial hepatectomy.
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IL-6 Promotes compensatory liver regeneration in cirrhotic rat after partial hepatectomy.

机译：IL-6促进部分肝切除术后肝硬化大鼠的代偿性肝再生。

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摘要

Major hepatic resection in cirrhotic patients is associated with impaired liver regeneration and failure, leading to high peri-operative mortality. In this work, the causes of defective regeneration in cirrhotic liver and the utility of IL-6 treatment were investigated in an experimental model combining cirrhosis and partial hepatectomy in the rat. Relative to normal controls, decompensated cirrhotic animals showed decreased survival, while compensated cirrhotic animals showed similar survival but reduced hepatic DNA synthesis and newly regenerated liver mass amount. Defective liver regeneration was associated with a decrease in STAT3 and NF-kB activation, consistent with an increased accumulation of their respective inhibitors PIAS3 and IkBalpha, and with a decreased induction of Bcl-xL. Treatment with recombinant IL-6 enhanced survival of decompensated cirrhotic animals, while it did not affect survival of compensated cirrhotic animals but sustained liver regeneration, by restoring STAT3 and NF-kB activation and Bcl-xL induction to the levels found in normal controls. The pro-growth effects exerted by IL-6 treatment in cirrhotic liver were attained also at low, pharmacologically acceptable doses. In conclusion, our results suggest that IL-6 treatment may be therapeutic in major resection of cirrhotic liver.
机译：肝硬化患者的大面积肝切除与肝再生和衰竭相关，导致围手术期高死亡率。在这项工作中，在大鼠肝硬化和部分肝切除联合实验模型中研究了肝硬化肝再生不良的原因和IL-6治疗的实用性。相对于正常对照，失代偿的肝硬化动物表现出降低的存活率，而经代偿的肝硬化动物表现出相似的存活率，但是肝DNA合成减少并且新近再生的肝脏量。肝再生不良与STAT3和NF-kB激活减少有关，与它们各自的抑制剂PIAS3和IkBalpha的积累增加有关，与Bcl-xL的诱导减少有关。通过将STAT3和NF-kB激活以及Bcl-xL诱导恢复到正常对照中的水平，重组IL-6的治疗增强了失代偿性肝硬化动物的存活率，虽然它不影响代偿性肝硬化动物的存活率，但维持了肝脏的再生。在低药理学上可接受的剂量下，也可以通过IL-6治疗在肝硬化肝中发挥促生长作用。总之，我们的结果表明IL-6治疗可能在肝硬化大手术中具有治疗作用。

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