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Non-selective β-blockers reduce bacterial translocation by restoring gut barrier function during experimental cirrhosis
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DOI：10.1016/j.jhep.2026.07.019.png)
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Abstract
En 中文
• Sustained β-adrenergic signalling disrupts the multi-layer intestinal barrier in experimental cirrhosis. • Propranolol restores barrier integrity beyond haemodynamic effects and largely independent of microbiota changes. • β-adrenergic stimulation recapitulates barrier disruption in the absence of liver injury or dysbiosis. • β-adrenergic hyperstimulation drives bi-directional barrier failure: bacterial translocation and albumin leakage. • VE-cadherin destabilisation mediates gut-vascular barrier failure downstream of β-adrenoceptor activation.
Keywords:
Intestinal permeability
β-adrenergic stimulation
Endothelial barrier
Confocal laser endomicroscopy
Gut-liver axis
AF
ascitic fluid
AUC
area under the curve
β-ARs
β-adrenoceptors
BDL
bile duct ligation
GC
goblet cells
GOF
gain-of-function
GVB
gut-vascular barrier
MIVEC
mice intestinal vascular endothelial cells
ISO
isoproterenol
MLN
mesenteric lymph nodes
NSBB
non-selective beta-blockers
PBT
pathological bacterial translocation
Prop
propranolol
TJ
tight junctions
VE
vascular endothelial
IF
immunofluorescence
CLE
confocal laser endomicroscopy
LP
lamina propria
RM ANOVA
repeated measures ANOVA
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