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  • Küçük Resim
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    Blocking VEGF by Bevacizumab Attenuates VEGF-Induced Vasospasm After Experimental Subarachnoid Hemorrhage in Rabbits
    (Elsevier Science Inc, 2020) Akturk, Umut Dogu; Tuncer, Cengiz; Bozkurt, Huseyin; Sahin, Omer Selcuk; Bulut, Husamettin; Arikok, Ata; Turkoglu, Erhan
    OBJECTIVE: Vasospasm after subarachnoid hemorrhage (SAH) plays a vital role in the development of delayed cerebral ischemia. Anti-vascular endothelial growth factor (VEGF) antibodies, like bevacizumab (BEV), may attenuate VEGF-stimulated angiogenesis, reduced vascular cell proliferation, and improve vasospasm after SAH. METHODS: Thirty-two adult male New Zealand white rabbits were randomly divided into 4 groups of 8 rabbits in each group: group 1 (control); group 2 (SAH); group 3 (SAH + vehicle); and group 4 (SAH + BEV). BEV (5 mg/kg, intraperitoneally) was administered 5 minutes after the intracisternal blood injection and continued for 72 hours once per day in the same dose for group 4. Animals were sacrificed 72 hours after SAH. Basilar artery cross-sectional areas, arterial wall thicknesses, and hippocampal degeneration scores were evaluated in all groups. RESULTS: VEGF is associated with the narrowing of the basilar artery. Treatment with BEV statistically significantly increased the cross-sectional area of the basilar artery when compared with the SAH and the vehicle groups. Basilar artery wall thicknesses in the BEV group was statistically significant smaller than in the SAH and vehicle groups. The hippocampal degeneration scores for the BEV and control groups were similar and significantly lower than those for the SAH and vehicle groups. CONCLUSIONS: Cellular proliferation and subsequent vessel wall thickening is a reason to delay cerebral ischemia and deterioration of the neurocognitive function. Intraperitoneal administration of BEV was found to attenuate cerebral vasospasm and prevent delayed cerebral ischemia and improve neurocognitive function after SAH in rabbits.
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    Öğe
    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.