BCL-3 Promotes Intracerebral Hemorrhage Progression by Increasing Blood–Brain Barrier Permeability, Inflammation, and Cell Apoptosis via Endoplasmic Reticulum Stress

Figure 1

ICH in vivo model construction. (a) EBD extravasation in sham, ICH-24 h, and ICH-72 h. (b) H&E staining demonstrating the histopathology of sham, ICH-24 h, and ICH-72 h. (c) The tight junction proteins of occludin and claudin-5 as assessed by TUNEL staining. DAPI, blue; occludin and claudin-5, red. (d, e) qPCR and western blotting performed on sham, ICH-24 h, and ICH-72 h. (f) The inflammation factors of IL-1, IL-6, and TNF-α in the serum of sham, ICH-24 h, and ICH-72 h were evaluated.