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    Biochanin A restored the blood-brain barrier in cerebral ischemia-reperfusion in rats
    (Assoc Medica Brasileira, 2024) Karaaslanli, Abdulmutalip; Asir, Firat; Gursoy, Gorkem Tutal; Tuncer, Mehmet Cudi
    OBJECTIVE: Blood-brain barrier is a protective layer that regulates the influx and efflux of biological materials for cerebral tissue. The aim of this study was to investigate the effects of Biochanin A on cerebral histopathology and blood-brain barrier immunohistochemically. METHODS: A total of 24 rats were assigned to three groups: sham, ischemia-reperfusion, and ischemia-reperfusion+Biochanin A. Ischemiareperfusion was performed by occluding the left carotid artery for 2/24 h. Notably, 20 mg/kg Biochanin A was administered to rats for 7 days after ischemia-reperfusion. Blood was collected for malondialdehyde and total oxidant/antioxidant status analysis. Cerebral tissues were processed for histopathology and further for immunohistochemical analysis. RESULTS: Malondialdehyde content with total oxidant status value was significantly increased and total antioxidant status values were significantly decreased in the ischemia-reperfusion group compared with the sham group. Biochanin A treatment significantly improved scores in the ischemiareperfusion+Biochanin A group. The normal histological appearance was recorded in the cerebral sections of the sham group. Degenerated neurons and vascular structures with disrupted integrity of the cerebral cortex were observed after ischemia-reperfusion. Biochanin A alleviated the histopathology in the cerebrum in the ischemia-reperfusion+Biochanin A group. Ischemia-reperfusion injury decreased the expression of blood-brain barrier in the ischemia-reperfusion group compared to the sham group. Administration of Biochanin A upregulated the blood-brain barrier immunoreactivity in the cerebrum by restoring blood-brain barrier. CONCLUSION: Cerebral ischemia-reperfusion caused an increase in oxidative stress and pathological lesions in the cerebrum. Biochanin A treatment restored the adverse effects of ischemia-reperfusion injury by restoring blood-brain barrier.
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    Gallic acid showed neuroprotection against endoplasmic reticulum stress in rats
    (Acta Cirurgica Brasileira, 2025) Karaaslanli, Abdulmutalip; Tuncer, Mehmet Cudi; Asir, Firat; Korak, Tugcan
    Purpose: We aimed to investigate the role of gallic acid treatment on spinal cord tissues after spinal cord injury (SCI) and its relationship with endoplasmic reticulum (ER) stress by histochemical, immunohistochemical, and in-silico techniques. Methods: Thirty female Wistar albino rats were divided into three groups: sham, SCI, and SCI+gallic acid. SCI was induced by dropping a 15-g weight onto the exposed T10-T11 spinal cord segment. The SCI+gallic acid group received 25 mg/kg of gallic acid intraperitoneally daily for one week. Histopathological, immunohistochemical, and silico analyses were performed. Results: Histological analysis revealed improved neural cell survival and tissue integrity in the SCI+gallic acid group compared to the SCI group. Caspase-12 expression was significantly increased in the SCI group, indicating elevated ER stress and apoptosis. Gallic acid treatment resulted in a marked reduction in caspase-12 expression in neurons, neuroglia, and endothelial cells, suggesting decreased ER stress. Conclusion: Gallic acid exhibits significant neuroprotective effects against ER stress and cellular damage in a rat model of SCI. The in-silico analysis revealed apoptotic and immune-related pathways in which gallic acid showed neuroprotective effects by regulating caspase-12. These results suggest that gallic acid may be a promising therapeutic agent for mitigating secondary damage post-SCI.