Department of Surgery I, School of Medicine, Complutense University of Madrid, Plaza de Ramón y Cajal s.n, 28040, Madrid, Spain.
Dig Dis Sci. 2011 Aug;56(8):2309-17. doi: 10.1007/s10620-011-1625-y. Epub 2011 Feb 24.
Hepatic encephalopathy is a syndrome whose physiopathology is poorly understood; therefore, current diagnostic tests are imperfect and modern therapy is nonspecific. Particularly, it has been suggested that inflammation plays an important role in the pathogenesis of portal hypertensive encephalopathy in the rat.
We have studied an experimental model of portal hypertension based on a triple partial portal vein ligation in the rat to verify this hypothesis.
One month after portal hypertension we assayed in the splanchnic area (liver, small bowel and mesenteric lymph nodes) and in the central nervous system (hippocampus and cerebellum) fractalkine (CX3CL1) and stromal cell-derived factor alpha (SDF1-α) as well as their respective receptors (CX3CR1 and CXCR4) because of their key role in inflammatory processes.
The significant increase of fractalkine in mesenteric lymph nodes (P<0.05) and its receptor (CX3CR1) in the small bowel (P<0.05) and hippocampus (P<0.01), associated with the increased expression of SDF1-α in the hippocampus (P<0.01) and the cerebellum (P<0.01) suggest that prehepatic portal hypertension in the rat induces important alterations in the expression of chemokines in the gut-brain axis.
The present study revealed that portal hypertension is associated with splanchnic-brain inflammatory alterations mediated by chemokines.
肝性脑病是一种发病机制尚不完全清楚的综合征；因此，目前的诊断测试并不完善，现代治疗也没有针对性。特别是，有人提出炎症在门静脉高压性脑病大鼠发病机制中起重要作用。
我们研究了一种基于大鼠三重部分门静脉结扎的门静脉高压实验模型，以验证这一假说。
门静脉高压 1 个月后，我们在大鼠内脏区（肝脏、小肠和肠系膜淋巴结）和中枢神经系统（海马体和小脑）中检测了趋化因子 fractalkine (CX3CL1) 和基质细胞衍生因子 alpha (SDF1-α) 及其各自的受体 (CX3CR1 和 CXCR4)，因为它们在炎症过程中起着关键作用。
肠系膜淋巴结 fractalkine 的显著增加（P<0.05）及其受体（CX3CR1）在小肠（P<0.05）和海马体（P<0.01）的增加，与海马体（P<0.01）和小脑（P<0.01）中 SDF1-α的表达增加相关，提示大鼠前肝门静脉高压诱导了肠-脑轴中趋化因子表达的重要改变。
本研究表明，门静脉高压与通过趋化因子介导的内脏-大脑炎症改变有关。
