Kupffer cells depletion alters cytokine expression and delays liver regeneration after Radio-frequency-assisted Liver Partition with Portal Vein Ligation.
Kupffer cells depletion alters cytokine expression and delays liver regeneration after Radio-frequency-assisted Liver Partition with Portal Vein Ligation.
复制标题
门静脉结扎射频辅助肝脏分割后，库普弗细胞耗竭会改变细胞因子表达并延迟肝脏再生。
DOI：
10.1016/j.molimm.2022.02.016
复制
发表时间：
2022
影响因子：
3.6
通讯作者：
Pei
中科院分区：
文献类型：
--
作者：
Weikang Zhang;Xi;Yong Tang;Jin;Chunmu Miao;J. Gong;Pei
在人类中，与分期肝切除术（ALPPS）的相关肝脏分割和门静脉结扎相比，射频辅助肝脏分割和门静脉结扎（RALPP）诱导的肝脏残留物肥大相当。然而，与ALPPS相比，它是否有明显改善尚不清楚，RALPP后肝再生的潜在机制需要进一步研究。本研究拟建立一种模拟RALPP的动物模型，探讨其肝再生机制。RALPP组在第一次手术后2 d内行肝脏射频消融和90%门静脉结扎术（PVL），并切除靶肝。ALPPS组行90%PVL+肝实质横断。对照组仅行射频消融（RAF组）、PVL（PVL组）或小左外侧叶切除（LLL组）。通过肝重和增殖相关分子评估肝再生。研究枯否细胞（KCs）在RALPP后肝再生中的作用。结果表明，与ALPPS相比，RALPP诱导了相当的肝再生，但小鼠的肝损伤和死亡率较低。与PVL相比，RALPP导致循环血浆中TNF-α和IL-6的过度表达。肝组织中浸润的KCs是RALPP组小鼠的特征。KCs耗竭显著抑制细胞因子表达，延迟RALPP后的肝再生。这些结果表明，RALPP在小鼠中诱导类似于ALPPS的加速肝再生，但比ALPPS更安全。KCs耗竭改变了RALPP后细胞因子的表达并延迟了肝再生。
Radio-frequency-assisted Liver Partition with Portal Vein Ligation (RALPP) induces comparable hypertrophy of the liver remnant compared to Associating Liver Partition and Portal vein ligation for Staged hepatectomy (ALPPS) in humans. However, whether it is significantly improved compared to ALPPS is unclear, and the underlying mechanisms of liver regeneration after RALPP need to further investigate. The present study was to develop an animal model mimicking RALPP and explore mechanisms of liver regeneration. The mice in RALPP group received liver radiofrequency ablation and 90% portal vein ligation (PVL), followed by resection of the targeted liver within two days after the first surgery. The mice in ALPPS group underwent 90% PVL combined with parenchyma transection. Controls received liver radiofrequency ablation (RAF group) or PVL (PVL group) or small left lateral lobe (LLL group) resection alone. Liver regeneration was assessed by liver weight and proliferation-associated molecules. The role of Kupffer cells (KCs) in liver regeneration was investigated after RALPP. The results showed that RALPP induced comparable liver regeneration compared to ALPPS, but with less liver injury and mortality in mice. RALPP led to over-expression of TNF-α and IL-6 in the circulating plasma compared with PVL. KCs infiltrating in liver tissues was a characteristic of mice in the RALPP group. KCs depletion markedly depressed cytokine expression and delayed liver regeneration after RALPP. These results suggested that RALPP in mice induced accelerated liver regeneration similar to ALPPS, but safer than ALPPS. KCs depletion altered cytokine expression and delayed liver regeneration after RALPP.