Sürdürülebilir Kalkınma Amaçları
Yayınlar
- MakaleYalnız künye2026Scopus SJRQ2In 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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İncele - MakaleAçık Erişim2025Scopus SJRQ1The 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.
AtıfScopus4WoS3OpenAlex3İncele - MakaleAçık Erişim2025Scopus SJRQ1The 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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