Fibroblast growth factor-2 prevents synaptic pathology in minimal
hepatic encephalopathy via NRG1/ErbB4 signaling
Abstract
Background and Purpose: Minimal hepatic encephalopathy (MHE) is
implicated in the impairment of memory function. Fibroblast growth
factor-2 (FGF2) is involved in modulating synaptic and neuronal
formation. Experimental Approach: The aim of this study is to examined
the impacts of FGF2 on MHE pathology. Our study addressed whether FGF2
could trigger neuregulin 1 (NRG1) release to ameliorate synaptic
impairment in MHE rats and in primary cultured neurons. Key Results: The
results showed the decreased FGF2 expression in MHE brains. After
treatment with FGF2, secreted neuregulin 1 (NRG1) and ErbB4 were
increased, and the interaction of the 2 proteins was enhanced.
Additionally, treatment with FGF2 or NRG1 induced synaptic formation,
with increase in the activity of synapse and the density of dendritic
spine, through Sirt1. NRG1 signaling was prevented by administration of
FGF2, which acts through the FGFR1 in MHE rats. Finally,
intracerebroventricular injection with FGF2 or NRG1 mitigated the
impairment of synaptogenesis. Conclusions and Implications: The data
suggest that FGF2 may be a promising latent therapeutic reagent for MHE
pathogenesis.