Browsing by Author "Tuncer, Mehmet Cudi"

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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.
Silymarin Protected the Cerebral Tissue From Endoplasmic Reticulum Stress
(Via Medica, 2025) Karaaslanli, Abdulmutalip; Tuncer, Mehmet Cudi; Asir, Firat; Korak, Tugcan
Background: Our aim is to explore silymarin's protective effects against endoplasmic reticulum (ER) stress via protein kinase R-like endoplasmic reticulum kinase (PERK) modulation, and elucidate potential enriched pathways through in silico analysis of silymarin-associated PERK protein interactors in cerebral ischaemia-reperfusion (IR) injury. Materials and methods: 30 rats were categorized into three groups: sham, IR, and IR + silymarin. Cerebral IR damage was not induced. Only the MCA was identified and clamped without further intervention. The sham group received only physiological serum intravenously. In the IR group, rats were exposed to 2 hours ischaemia and then 3 hours of reperfusion. In the IR + silymarin group the rats received 1 mu g/kg silymarin intravenously (i.v.) before induction of cerebral IR. Cerebral tissues were processed for histological tissue preparation. Haematoxylineosin and PERK immunostaining were applied. In Cytoscape software, we imported and integrated the silymarin and PERK protein-protein interaction networks generated from the STITCH and STRING databases, respectively. Subsequently, Reactome pathway annotation was performed for this intersected network. Results: In the sham group, neurons were large and round with oval nuclei, and no histopathological changes were observed. In the IR group, neurons and neuroglial cells showed degeneration with pyknotic nuclei, apoptotic bodies, dilated and congested cerebral capillaries, and numerous vacuoles. After silymarin treatment, the IR + silymarin group showed a restoration of normal histology, with more regular neural and neuroglial cells and decreased vessel dilation and congestion. PERK immunoexpression was mainly negative in the sham group, increased in the IR group, and decreased again in the IR + silymarin group. Upon intersecting the interactors of silymarin and PERK, 17 common proteins were identified. Reactome pathway analysis revealed potential impacts of these proteins on key pathways including immune and cytokine signaling, apoptosis, estrogen signaling, and extracellular matrix degradation. Conclusions: Silymarin's targeting of PERKoffers a promising approach to alleviate ER stress and potentially modulate multiple critical pathways in cerebral ischaemia reperfusion, serving as a comprehensive therapeuticstrategy for managing cerebral IR injury. (Folia Morphol 2025; 84, 3: 534-543)