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. Author manuscript; available in PMC: 2015 Jun 1.
Published in final edited form as: Dig Liver Dis. 2014 Mar 12;46(6):527–534. doi: 10.1016/j.dld.2014.01.159

Figure 1.

Figure 1

Cholestasis leads to blood brain barrier permeability via circulating factors. (A) Permeability of the blood brain barrier was assessed via an Evan’s blue assay in sham and bile duct ligated rats 5 days post-surgery. BDL rats have a significant increase in blood brain barrier permeability compared to sham rats. (* denotes p<0.05, n=4) (B) Brain slices of sham and bile duct ligated rats were stained with a SMI-71 antibody (red) allowing for microvessel visualization and counterstained with DAPI (blue). Sham rats have long continuous staining of microvessels with several branch points (white arrows). Bile duct ligated rats show dispersed staining, indicating a loss of microvessel integrity. Scale bar represents 100μm. (C) Albumin immunoreactivity was assessed in sham and Bile duct ligated rats via immunohistochemistry. Bile duct ligated rats have a higher degree of albumin immunoreactivity in brain slices, particularly the hippocampus and the cortex compared to sham operated rats, indicating a loss of blood brain barrier integrity. (D) Confluent monolayers of brain endothelial cells were treated for 24 hours with serum extracted from either sham or bile duct ligated rats 5 days post-surgery and permeability was measured via the passive diffusion of 10kDa fluorescein isothiocyanate-dextran. Monolayers treated with various concentrations of bile duct ligated serum have increased permeability compared to 75% sham serum. (* denotes p<0.05, n=6) Data are expressed as average permeability coefficient ± SEM. (BDL; bile duct ligation, HP; hippocampus, CTX, cortex)