The present study revealed that portal hypertension is associated with splanchnic-brain inflammatory alterations mediated by chemokines.

Combined approach therapy of PDT + ALN 0.25 mg/kg demonstrated a protective effect on alveolar bone loss.

Brain ischaemia and reperfusion produce alterations in the microenvironment of the parenchyma, including ATP depletion, ionic homeostasis alterations, inflammation, release of multiple cytokines and abnormal release of neurotransmitters. As a consequence, the induction of proliferation and migration of neural stem cells is redirected towards the peri-infarct region. The success of new neurorestorative treatments for damaged brain implies the need to describe with greater accuracy the mechanisms in charge of regulating adult neurogenesis, under both physiological and pathological conditions. Recent evidence demonstrates that many neurotransmitters, glutamate in particular, control the subventricular zone (SVZ), thus being part of the complex signal network that exerts a remarkable influence on the production of new neurones. Neurotransmitters provide a link between brain activity and SVZ neurogenesis. Therefore, a deeper knowledge of the role of neurotransmitters systems, such as glutamate and its transporters, in adult neurogenesis, may prove a valuable tool to be utilized as a neurorestorative therapy in this pathology.

In experimental portal hypertension, the inflammatory cerebral-splanchnic axis alterations could be mediated by chemokines. In Wistar rats with partial portal vein ligation, RANTES, CXCR4/SDF-1alpha and CX3CR1/Fractalkine were measured in several brain and gastrointestinal areas. Nestine and Bcl-2 were assayed in the hippocampus, and TNF- in the liver, ileum and mesenteric lymph nodes. In the CNS of portal hypertensive-rats, SDF-1alpha increased in the hippocampus (p<0.05), and cerebellum (p<0.05), and RANTES (p<0.05) decreased in the striatum. TNF-alpha and CXCR4 increased in the hippocampus and TNF-alpha in the ileum and in mesenteric lymphatic nodes. CX3CR1 increased in the ileum (p<0.05), whereas Fractalkine increased (p<0.05) in the mesenteric lymph nodes. Splanchnic CX3CR1 and fractalkine overexpression may suggest the development of anti-inflammatory and repair mechanisms to balance pro-inflammatory mechanisms. SDF1-alpha upregulation in the CNS could suggest its involvement in neuronal remodeling. The existence of a communication mechanism chemokinedependent through the splanchnic-brain axis in portal hypertension could be hypothesized.