The gut-brain axis plays a potential role in numerous physiological and pathological conditions. In particular, there are several substances and a dense neuronal network that link stomach with Central Nervous System (CNS). Several communication mechanisms involve spinal and vagal system. In particular, hypothalamo-pituitary-adrenocortical (HPA) axis, thyrotropin-releasing hormone (TRH)-containing nerve fibers and capsaicin-sensitive nerves are principal mediators of the harmful and protective CSN-mediated effects on gastric mucosa. Also, existing evidence indicates that nitric oxide (NO), prostaglandins (PGs) and calcitonin gene-related peptide (CGRP) play a role as final effectors of gastric protection. This review is focused on the role of gut-brain axis in gastric damage and protection and, in particular, on the role of steroids, TRH, PGs, melatonin, hydrogen sulfide (H2S) and peptides influencing food intake (leptin, cholecystokinin (CCK), peptide YY, central glucagon-like peptide-1 [GLP-1], ghrelin). Also, the role of GABAergic and glutamatergic pathways in gastric mucosal protection have been examined.

Gut-Brain Axis in Gastric Mucosal Damage and Protection

CAPUANO, Annalisa;FEDERICO, Alessandro;ROMANO, Marco
2016

Abstract

The gut-brain axis plays a potential role in numerous physiological and pathological conditions. In particular, there are several substances and a dense neuronal network that link stomach with Central Nervous System (CNS). Several communication mechanisms involve spinal and vagal system. In particular, hypothalamo-pituitary-adrenocortical (HPA) axis, thyrotropin-releasing hormone (TRH)-containing nerve fibers and capsaicin-sensitive nerves are principal mediators of the harmful and protective CSN-mediated effects on gastric mucosa. Also, existing evidence indicates that nitric oxide (NO), prostaglandins (PGs) and calcitonin gene-related peptide (CGRP) play a role as final effectors of gastric protection. This review is focused on the role of gut-brain axis in gastric damage and protection and, in particular, on the role of steroids, TRH, PGs, melatonin, hydrogen sulfide (H2S) and peptides influencing food intake (leptin, cholecystokinin (CCK), peptide YY, central glucagon-like peptide-1 [GLP-1], ghrelin). Also, the role of GABAergic and glutamatergic pathways in gastric mucosal protection have been examined.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11591/364574
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