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    Potential use of decorin in preventing cerebral vasospasm through the inhibition of transforming growth factor-beta activity: Insights from an experimental rabbit subarachnoid hemorrhage model
    (Elsevier Inc., 2025) Yaman, Betul; Gel, Gulce; Tuncer, Cengiz; Hanalioglu, Sahin; Bulut, Husamettin; Arikök, Ata Türker; Gürer, Bora
    Objective: The development of vasospasm after subarachnoid hemorrhage (SAH) is a major cause of death and disability. It leads to structural changes such as smooth muscle and myofibroblast proliferation, necrosis, intimal hyperplasia, and vascular fibrosis. Transforming growth factor-beta1 (TGF-β1) activates nonmuscular myofibroblasts, promoting cerebral vasoconstriction. Decorin, a natural TGF-β inhibitor, has not yet been evaluated for its potential to prevent SAH-induced vasospasm. This study aimed to investigate the effects of decorin on cerebral vasculopathy and hippocampal injury in a rabbit model of TGF-β-induced vasospasm. Methods: Thirty-two male New Zealand white rabbits (2.5–4 kg) were randomly assigned to four groups: control, SAH, decorin, and TGF-β1. Except for the control group, all underwent the SAH procedure. The decorin group received 100 μg/kg decorin intraperitoneally for 3 days; the TGF-β1 group received 50 μg TGF-β1 intracisternally in 1 cc autologous CSF. Animals were sacrificed at 72 h using perfusion–fixation. Basilar artery cross-sectional area, wall thickness, and hippocampal degeneration scores were assessed using histopathological and statistical analysis systems. Results: Based on statistical analyses, decorin treatment significantly increased the cross-sectional area of the basilar artery but significantly reduced the wall thicknesses compared with those in the SAH and TGF-β1 groups. Furthermore, hippocampal neuronal degeneration scores were significantly lower in the decorin and control groups than in the SAH and TGF-β1 groups. There were no significant differences between the groups in terms of proliferating cell nuclear antigen. Conclusion: Decorin treatment in rabbits with experimentally induced SAH ameliorated TGF-β1-induced vasospasm, cerebral vasculopathy associated with vascular wall fibrosis, and subsequent decreased vessel wall thickness. © 2025 Elsevier B.V., All rights reserved.