Clinical and experimental study of regeneration of nonembolized lobe after portal vein embolization

门静脉栓塞术后非栓塞肺叶再生的临床及实验研究

基本信息

批准号：
13671297
负责人：
NAGINO Masato
金额：
$ 1.92万
依托单位：
Nagoya University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2002
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13671297/
关键词：
Portal vein embolization Portal blood flow Liver regeneration Interleukin-6 Endothelial cell Stretch stress TNF-α NF κ B 門脈内皮ストレッチ門脈内径

项目摘要

This study demonstrated possible mechanism of liver regeneration in the nonembolized lobe after portal vein embolization. Clinical study : After right portal vein embolization, the blood flow of the left portal vein significantly increased, and the diameter of this vein also enlarged. Ultrasonographic measurement revealed that right portal vein embolization induces approximately 150% increase in diameter of the segment 2, segment 3, and segment 4 portal branches. Serum interleukin-6 concentrations significantly increased within 3 hours after portal vein embolization, peaked at 24 hours, then gradually decreased. The concentrations of tumor necrosis factor (TNF)-α and hepatocyte growth factor (HGF) remained unchanged. Experimental study : Human liver sinusoidal microvascular endothelial cells (HLSECs) and human umbilical vein endothelial cells (HUVECs) were cultured on the silicon chamber which were 150% stretched over the entire membrane. After this continuous mechanical stretch, the concentration of interleukin-6 in the supernatant of endothelial cells significantly increased, while the concentrations of TNF-α and HGF were unchanged. Interleukin-6 mRNA expression followed activation of NF κ B. Conclusion : These findings indicate that portal vein embolization dilates the portal branches in the nonembolized lobe, exposing hepatic vasculature to stretch stress. This hemodynamic change may act as a trigger for interleukin-6 release from endothelial cells and contribute to the activation of regenerative cascade in the nonembolized lobes.

这项研究证明了门静脉栓塞后未栓塞叶中肝脏再生的可能机制。临床研究：右门静脉栓塞后，左门静脉的血流显着增加，并且该静脉的直径也增加了。超声测量表明，右门静脉栓塞会影响分段2，段3和第4个门户分支的直径大约增加150％。血清白介素6浓度在门静脉栓塞后3小时内显着增加，在24小时以峰值达到峰值，然后逐渐降低。肿瘤坏死因子（TNF）-α和肝细胞生长因子（HGF）的浓度保持不变。实验研究：在整个膜上在整个膜上延伸150％的硅腔室，在硅腔室上培养了人类肝脏的微血管内皮细胞（HLSEC）和人脐静脉内皮细胞（HUVEC）。在这种连续的机械拉伸之后，内皮细胞上清液中白介素-6的浓度显着增加，而TNF-α和HGF的浓度不变。白介素-6 mRNA表达在激活NFκB之后。结论：这些发现表明，门静脉栓塞扩张了未膨胀的叶片中的门户分支，使肝脉管系统暴露于拉伸应力。血液动力学变化可能充当白介素6从内皮细胞释放的触发因素，并有助于非栓塞爱的再生级联反应的激活。