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• MakaleAçık Erişim2026/r/gumushane/13908
  Electric field–induced inflammatory and angiogenic responses in rat female reproductive tissues: evidence for early extracellular matrix remodeling

  Ozmen, Ozlem; Asci, Halil; Kolay, Oznur; Selcuk, Elif Nur; Yuksel, Duygu; Comlekci, Selcuk; Karabacak, Pinar

  High-intensity electric fields (EFs) are increasingly encountered in occupational and environmental settings, raising concerns regarding their potential biological effects on hormonally responsive organs. However, the cellular and molecular responses of female reproductive tissues to short-term exposure to high-voltage EFs remain insufficiently characterized. This study aims to investigate EF-associated histopathological and immunohistochemical alterations in major female reproductive organs. Forty adult female Wistar albino rats were randomly assigned to five experimental groups (n = 8 per group): a control group (0 min) and four EF-exposed groups subjected to a nominal electric field intensity of 10 kV/m EF for 1, 5, 15, or 30 min using a custom-designed parallel-plate exposure system. The field intensity was verified at predefined measurement points within the exposure setup. Ovaries, uterus, and uterine tubes were examined using hematoxylin–eosin staining and semi-quantitative histopathological scoring. Immunohistochemical analyses were performed to evaluate the expression of tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), and osteonectin as markers of inflammation, angiogenesis, and extracellular matrix remodeling. Exposure to the electric field was associated with time-dependent histopathological alterations, including tissue edema, hemorrhage, epithelial degeneration, and leukocyte infiltration. The most pronounced ovarian and uterine changes were observed in the 30-min exposure group, whereas the uterine tubes exhibited comparatively milder structural alterations. Immunohistochemical analysis demonstrated increased TNF-α and VEGF expression in higher-exposure groups, suggesting activation of inflammatory and angiogenic pathways. Osteonectin expression was elevated in all examined reproductive tissues and was also detected in regions without overt morphological damage, indicating its potential sensitivity to early tissue stress responses associated with EF exposure. Significant correlations were observed between histopathological injury scores and immunohistochemical marker expression levels. Overall, short-term exposure to high-intensity electric field was associated with inflammatory signaling, angiogenic responses, and extracellular matrix remodeling in female reproductive tissues in this experimental model. These findings provide histological and immunohistochemical evidence of tissue responses to EF exposure and underscore the need for further studies incorporating comprehensive exposure characterization and additional molecular endpoints to better define potential reproductive health implications to high-voltage electric fields.

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• MakaleYalnız künye2026/r/gumushane/13698
  In sepsis-associated cardiotoxicity, remifentanil reduces oxidative stress, inflammation, and apoptosis to maintain mitochondrial biogenesis by inhibiting NFkB and cas-3 immunoexpressions and enhancing SIRT1 upregulation

  Tepebaşi, Muhammet Yusuf; Aşci, Halil; Selçuk, Esma; Uysal, Dinçer; Bindal, Ahmet; Yüksel, Duygu; Özmen, Özlem

  Objective: Sepsis-induced cardiotoxicity (SIC) is a critical complication characterized by inflammation, oxidative stress, and apoptosis, leading to myocardial dysfunction. The short-acting opioid analgesic remifentanil (REMI) possesses antioxidant and anti-inflammatory properties. This study aimed to evaluate the cardioprotective effects of REMI on lipopolysaccharide (LPS)-induced SIC by examining inflammation, oxidative stress, apoptosis, and mitochondrial function. Materials and methods: Thirty-two female Wistar albino rats were divided into four groups: control, lipopolysaccharide (LPS), LPS+REMI, and REMI. Myocardial and aortic tissues were analyzed for histopathology, immunoexpression of Caspase-3 (Cas-3), nuclear factor kappa beta (NF-κB), and tumor necrosis factor alpha (TNF-α). Oxidative stress markers, including total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI), were measured. Mitochondrial apoptosis-related gene expression of AMP-activated protein kinase (AMPK), BCL2 Associated X (BAX), B-cell lymphoma 2 (BCL-2), Sirtuin 1 (SIRT1), and Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) was assessed. Results: LPS administration induced severe histopathological damage, increased oxidative stress (elevated TOS and OSI), and upregulated apoptotic (Cas-3, BAX/BCL-2 imbalance) and inflammatory (NF-κB, TNF-α) markers. REMI treatment significantly alleviated myocardial and aortic injury, reducing the histopathological score. It markedly decreased Cas-3, NF-κB, and TNF-α expression, lowered TOS and OSI levels, and modulated the BAX/BCL-2. Furthermore, REMI restored the expression of AMPK, SIRT1, and PGC-1α genes, indicating a protective effect on mitochondrial biogenesis and energy metabolism. Conclusions: REMI exhibits significant cardioprotective effects in LPS-induced SIC by attenuating inflammation, oxidative stress, and apoptosis while preserving mitochondrial homeostasis.

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• MakaleAçık Erişim2025/r/gumushane/14325
  The Protective Effect of Boric Acid Against High Fructose-Induced Liver and Kidney Damage in Rats

  Yüksel, Duygu; Başeğmez, Mehmet; Kan, Fahriye

  This study aimed to determine the protective role of boric acid (BA) in high fructose (HF)-induced liver and kidney toxicity in a young rat model. High-fructose consumption causes serious damage to liver and kidney tissue in healthy individuals and contributes to the emergence of various metabolic diseases. Thirty-two healthy female Wistar albino rats (250–300 g weight and 3–4 months) were randomly distributed into four equal groups (n = 8): control, high fructose % 20 (HF), boric acid 20 mg/kg (BA), and HF + BA. High fructose was freshly prepared and administered to the rats as 20 g of d-fructose dissolved in 100 mL of tap water daily for a duration of 30 days. Boric acid (20 mg/kg) was administered through gastric gavage throughout the 30-day study period. At the end of study, blood, liver, and kidney were collected from rats. The results indicated that high fructose induced increased glucose, total cholesterol, triglyceride, and urea levels in rat serum. Boric acid administration significantly decreased glucose, total cholesterol, triglyceride, and urea levels in HF + BA groups. The results indicated that high fructose-induced oxidative stress by increasing the level of MDA and by decreasing GSH levels, and CAT activity in the liver and kidney of rats. However, oral BA administration significantly decreased MDA levels and increased GSH levels, and CAT activity (p < 0.05). Furthermore, BA significantly reduced high fructose-induced histopathological and Immunohistochemistry alteration in the liver and kidney tissues. In conclusion, BA may prevent the oxidative imbalance and histopathological and immunohistochemical damage caused by high fructose in liver and kidney tissues in rats.

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• MakaleAçık Erişim2025/r/gumushane/14238
  The Effect of Boric Acid on Oxidative Stress, Inflammation, and Apoptosis in Embryonic and Fetal Tissues Damage Caused by Consumption of High-Fructose Corn Syrup in Pregnant Rats

  Başeğmez, Mehmet; Yüksel, Duygu

  This study aimed to determine the protective role of boric acid in a pregnant rat model of high fructose corn syrup consumption. Consumption of high fructose corn syrup has been associated with adverse health outcomes in humans and animals. Twenty-eight healthy female Wistar albino rats (250–300 g weight and 16–24 weeks old) were randomly distributed into four equal groups (n = 7): Control, Boric acid (BA), High Fructose Corn Syrup (HFCS), HFCS + BA. Boric acid (20 mg/kg) was administered to pregnant rats via oral gavage every day during pregnancy. The prepared 30% HFCS (F30) solution (24% fructose, 28% dextrose) was added to the drinking water throughout pregnancy. At the end of pregnancy (day 19), blood, placenta, uterus, and fetuses were collected from rats. The results indicated that HFCS increases oxidative stress by increasing the level of MDA and decreasing GSH, SOD, and CAT activity in the blood of maternal. However, BA administration significantly decreased MDA levels and increased GSH levels, SOD, and CAT activity (p < 0.05). In addition, HFCS consumption significantly increased plasma TNF-α, IL-6, and leptin levels compared to control, BA, and HFCS + BA groups (p < 0.05). However, BA administration significantly decreased plasma TNF-α, IL-6, and leptin levels (p < 0.05). Furthermore, BA (20 mg/kg) significantly decreased HFCS-induced histopathological and immunohistochemical alterations in the placenta, uterus, and fetal tissue. In conclusion, BA may prevent HFCS toxicity in maternal and fetal tissues, as it regulates oxidative imbalance in pregnant rat and alleviates histopathological and immunohistochemical changes. The findings indicate a need for further studies to assess the potential of boron in preventing or mitigating the effects of HFCS during pregnancy.

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• MakaleAçık Erişim2025/r/gumushane/14017
  Cardiovascular Findings and Effects of Caffeine on Experimental Hypothyroidism

  Yuksel, Duygu; Ozmen, Ozlem

  Background: Thyroid hormone deficiencies can disrupt organ functions, significantly impacting the cardiovascular system. Recently, the effects of thyroid hormones on the heart have garnered increased attention. However, most studies are conducted on humans using clinical data, while cellular-level and experimental studies remain limited. Objective: This study aimed to investigate the cardiovascular implications of hypothyroidism and evaluate the impact of caffeine on cardiac health in rats induced with hypothyroidism using propylthiouracil (PTU). Methods: The study involved 60 rats divided into six groups. Group 1 served as the untreated control. Group 2 received PTU for two months to induce hypothyroidism. Group 3 received PTU for one month, followed by caffeine for one month. Group 4 received caffeine for two months. Group 5 received both PTU and caffeine simultaneously for two months. Group 6 received PTU for one month, followed by one month under normal conditions. Results: During necropsy, normal thyroid glands were observed in Groups 1, 4, and 6, enlarged thyroids in Group 2, and smaller thyroids in Groups 3 and 5. Microscopic examination revealed varying thyroid histologies: Group 2 showed significant epithelial cell proliferation and absent colloid, while Groups 3, 5, and 6 had altered yet colloid-containing acini. Macroscopic inspection of hearts appeared normal across all groups. However, histopathological examination revealed significant hyperemia and microhemorrhages in Group 2, contrasting with normal findings in other groups. Immunohistochemical analysis indicated reduced cardiac troponin expression in Group 2, while other groups maintained prominent expression. Additionally, Group 2 displayed increased serum TSH levels and decreased T3 and T4 levels. Conclusion: The findings suggest that administering caffeine alongside or after PTU treatment in rats with experimentally induced hypothyroidism may ameliorate thyroid and cardiac irregularities. This study indicates caffeine's potential in mitigating the adverse effects of hypothyroidism on thyroid and heart health.

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