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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.

这项研究证实了门静脉栓塞术后非栓塞区肝脏再生的可能机制。临床研究：门静脉右支栓塞术后，门静脉左支血流量明显增加，且管径增大。超声测量显示，右门静脉栓塞术可导致门静脉2段、3段和4段门静脉分支直径增加约150%。门静脉栓塞术后3h内血清IL-6浓度显著升高，24小时达高峰，随后逐渐下降。血清肿瘤坏死因子-α和肝细胞生长因子水平无明显变化。实验研究：人肝窦微血管内皮细胞(HLSECs)和人脐静脉内皮细胞(HUVECs)在150%拉伸的硅胶室中培养。持续机械牵张后，内皮细胞培养上清液中IL-6浓度显著升高，而肿瘤坏死因子-α和肝细胞生长因子浓度无明显变化。结论：门静脉栓塞术使非栓塞区门静脉分支扩张，使肝血管处于张应力状态。这种血流动力学改变可能是内皮细胞释放白细胞介素6的触发因素，并有助于激活未经栓塞的肺叶再生级联反应。