Abstract
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-﷿a 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.
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