PubMed İndeksli Yayınlar Koleksiyonu
Permanent URI for this collectionhttps://hdl.handle.net/20.500.14720/6
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Browsing PubMed İndeksli Yayınlar Koleksiyonu by Publisher "Acta Cirurgica Brasileira"
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Article Caffeine Mitigates Tamoxifen-Induced Fatty Liver in Wistar Rats(Acta Cirurgica Brasileira, 2024) Sezgin, Yasin; Bora, Ejder Saylav; Arda, Duygu Burcu; Uyanikgil, Yigit; Erbas, OytunPurpose: Tamoxifen, a widely used drug for breast cancer treatment, is associated with adverse effects on the liver, including the development of fatty liver. This study aimed to investigate the potential protective effect of caffeine against tamoxifen-induced fatty liver in Wistar rats. Methods: Rats were divided into normal control, tamoxifen + saline, and tamoxifen + caffeine. Plasma samples were assessed for biochemical markers related to oxidative stress, inflammation, liver function, and cell damage. Additionally, liver histopathology was examined to quantify the extent of fatty infiltration. Results: In the tamoxifen + saline group, elevated levels of plasma malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-alpha), alanine aminotransferase (ALT), cytokeratin 18, and soluble ST2 were observed compared to the normal control group, indicating increased oxidative stress, inflammation, and liver injury (p < 0.01). Moreover, histopathological examination revealed a significant increase in fatty infiltration (p < 0.001). However, in the tamoxifen + caffeine group, these markers were markedly reduced (p < 0.05, p < 0.01), and fatty infiltration was significantly mitigated (p < 0.001). Conclusion: The findings suggest that caffeine administration attenuates tamoxifen-induced fatty liver in rats by ameliorating oxidative stress, inflammation, liver injury, and cell damage. Histopathological evidence further supports the protective role of caffeine. This study highlights the potential of caffeine as a therapeutic intervention to counter tamoxifen-induced hepatic complications, contributing to the optimization of breast cancer treatment strategies.Article Effect of Low- and High-Dose Methotrexate on Wound Healing in Rats(Acta Cirurgica Brasileira, 2025) Karasu, Abdullah; Kuscu, Yagmur; Kayikci, Caner; Yildirim, Serkan; Kuscu, Oguzhan; Kiliclioglu, MetinPurpose: To investigate the effect of intraperitoneal treatment with low- and high-dose methotrexate (MTX) on wound healing in rats. Methods: The study sample consisted of 54 healthy rats. Under aseptic conditions, skin wounds were created with two circular fullthickness punch tools, 10 mm in diameter, one on the right and the other one on the left of the dorsal vertebral line. The rats were randomly assigned to one of three main treatment groups. On the 0th day (2 hours before wound creation), 7th day, and 14th day, the control group received 0.3-mL saline, the low-MTX group received 3 mg/kg MTX, and the high-MTX group received 30 mg/kg MTX, all administered intraperitoneally. The wounds were evaluated seven, 14, and 21 days after injury through morphometrical, biochemical, histopathological, and immunohistochemical analyses. Results: MTX dose-dependently decreased the degree of inflammation and angiogenesis, tissue hydroxyproline level, and HSP70 and tumor necrosis factor-alpha expression in the early phase of wound healing. It also suppressed epithelialization and collagen 1 expression throughout the wound-healing process. Conclusion: The wounds treated with high-dose of MTX had statistically delayed wound closure on days 7, 14 and 21 compared to the saline group, while wounds treated with low-dose of MTX only had statistically delayed wound closure on day 14. In addition, weight loss was observed in rats treated with high-dose MTX, which was thought to reflect its toxicity. The dose-dependent adverse effect of MTX on wound healing may be due to its antiproliferative, antifibrotic, anti-inflammatory, and antiangiogenic effects.Article Gallic Acid Showed Neuroprotection Against Endoplasmic Reticulum Stress in Rats(Acta Cirurgica Brasileira, 2025) Karaaslanli, Abdulmutalip; Tuncer, Mehmet Cudi; Asir, Firat; Korak, TugcanPurpose: 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.Article New Determinants for Casual Peripheral Mechanism of Neurogenic Lung Edema in Subarachnoid Hemorrhage Due To Ischemic Degeneration of Vagal Nerve, Kidney and Lung Circuitry. Experimental Study(Acta Cirurgica Brasileira, 2019) Soyalp, Celaleddin; Kocak, Mehmet Nuri; Ahiskalioglu, Ali; Aksoy, Mehmet; Atalay, Canan; Aydin, Mehmet Dumlu; Ozmen, SevilayPurpose: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage. Methods: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded. Results: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm(2)), atrophic glomerulus density (n/mm(3)) and NLE scores of control, SHAM and study groups were estimated as 2.40 +/- 1.82, 2.20 +/- 1.30, 1.80 +/- 1.10, 8.00 +/- 2.24, 8.80 +/- 2.39, 4.40 +/- 1.14 and 154.38 +/- 13.61, 34.69 +/- 2.68 and 12.19 +/- 1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001). Conclusion: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.

