Salih Çibuk

Background: Lipoprotein metabolism, inflammation, and oxidative stress (OS) play interconnected roles in the pathogenesis of acute coronary syndrome (ACS). However, the relationship between oxidative stress biomarkers and coronary artery disease (CAD) complexity, particularly as assessed by the SYNTAX II score, remains incompletely understood. This study aimed to evaluate serum levels of oxidative stress–related biomarkers and to investigate their association with the SYNTAX II score in patients with newly diagnosed ACS. Methods: This was a retrospective, single-center observational study. A total of 60 patients with newly diagnosed ACS who underwent percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) were consecutively enrolled. Serum levels of superoxide dismutase (SOD), advanced oxidation protein products (AOPP), glutathione, catalase, and malondialdehyde (MDA) were measured using ELISA methods. Associations between oxidative stress markers and the SYNTAX II score were analyzed using correlation and regression analyses. Results: Median levels of SOD, AOPP, and glutathione were 261.0 (244.18–324.86) U/L, 23.81 (22.62–25.80) ng/mL, and 6.08 (5.28–11.46) ng/mL, respectively. Mean catalase and MDA levels were 339.07 ± 44.81 pg/mL and 0.66 ± 0.07 mmol/L. The SYNTAX II score was positively correlated with SOD, AOPP, glutathione, catalase, and MDA, as well as with age, female sex, and potassium levels, while it was negatively correlated with hemoglobin, creatinine clearance, and left ventricular ejection fraction (all p < 0.05). Patients with higher SYNTAX II scores demonstrated elevated levels of both oxidant and antioxidant biomarkers. Conclusions: Oxidative stress-related biomarkers were associated with the SYNTAX II score in patients with newly diagnosed ACS.

Background/Objectives: Autism spectrum disorder (ASD) is a neurodevelopmental condition increasingly associated with dysregulated neuroimmune signaling and altered neurotrophic homeostasis. Tumor necrosis factor-alpha (TNF-α) has been implicated in ASD pathophysiology; however, the downstream effects of TNF-α blockade on cytokine–neurotrophin interactions during neurodevelopment remain insufficiently characterized. In this study, we evaluated the effects of infliximab (IFX), a monoclonal anti-TNF-α antibody, on behavioral performance, neuroinflammatory cytokine profiles, glial activation, and brain-derived neurotrophic factor (BDNF) signaling in a propionic acid (PPA)-induced experimental ASD rat model. Methods: Experimental ASD was induced by propionic acid administration in rats. Animals were divided into control and treatment groups. Behavioral performance was assessed using the Morris Water Maze, direct social interaction, and three-chamber sociability tests. Levels of TNF-α, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and BDNF were measured in serum, hippocampal, and cerebellar tissues. Microglial and astrocytic activation were evaluated using CD11 and GFAP immunohistochemistry. Results: PPA administration resulted in pronounced impairments in learning, memory, and social behaviors, accompanied by elevated proinflammatory cytokine levels, increased BDNF expression, and marked glial activation in the hippocampus and cerebellum. Although IFX treatment significantly reduced TNF-α levels in central tissues, it did not improve behavioral deficits and was associated with persistently elevated IL-1β and IL-6 levels, sustained glial reactivity, and further alterations in BDNF levels. Conclusions: These findings suggest that TNF-α suppression alone does not normalize the disrupted cytokine–neurotrophin axis and may differentially modulate BDNF-related neuroplastic signaling during development. In conclusion, this study indicates that non-selective TNF-α blockade during neurodevelopment fails to confer behavioral benefit in experimental ASD and highlights the importance of considering cytokine–BDNF pathway interactions when designing immunomodulatory strategies for neurodevelopmental disorders.

Gentamicin (GM) is an aminoglycoside antibiotic widely used to treat gram-negative infections. Oxidative stress is known to play an important role in the nephrotoxicity of gentamicin. Therefore, the aim of this study was to investigate the possible protective effect of protocatechuic acid (PCA), which is believed to have antioxidant properties, on nephrotoxicity induced by gentamicin. For this purpose, 32 rats were randomly divided into four groups: control (oral physiological saline), PCA (20 mg/kg orally), GM (80 mg/kg/day/i.p.), GM+PCA (80 mg/kg/day/i.p. GM and 20 mg/kg PCA orally). The sampling period was eight days. Blood samples were collected for biochemical analysis and kidney samples for immunohistochemical and histopathological examination. Serum levels of urea, creatinine, Na, K and Cl were measured using an autoanalyzer, while analyses of malondialdehyde (MDA), advanced oxidation protein products (AOPP), gutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were analyzed by ELISA. While the values ​​of urea (p<0.001), creatinine (p<0.001), MDA (p<0.05) and AOPP (p<0.05) decreased in the GM+PCA group compared to the GM group, the values ​​of GSH (p<0.05) and GPx activity (p<0.05) increased. In conclusion, in GM-induced nephrotoxicity, PCA prevented lipid peroxidation and protein oxidation, increased GSH levels and GPx activity, and reduced tubular epithelial necrosis, glomerular atrophy, 8-OHdG and Kim-1 expression in renal cells, according to histopathological and immunohistochemical results. This study once again highlighted that PCA is a good antioxidant, and it can be said that PCA has a protective effect against nephrotoxicity caused by GM.

Objective: Metabolic syndrome is a disease characterized by hypertension, dyslipidemia and insulin resistance, and constitutes an important risk factor for cardiovascular disorders. The effect of evening primrose oil (EPO) on insülin, adiponectin and resistin levels in brain tissue was investigated in a fructose-related metabolic syndrome model. Materials and Methods: The rats were divided into 4 groups as control, evening primrose oil (orally at a dose of 0.1 ml/rat/day), fructose (20% fructose added), fructose+evening primrose oil for 57 days. At the end of the experiment, brain samples were taken and homogenized. Then, insülin, adiponectin and resistin levels were determined by ELISA. Results: Plasma insulin and resistin levels of the fructose group increased (p≤0.05 ) compared to the controls, on the contrary, adiponectin levels were significantly decreased (p≤0.05 ) in the fructose group. When EPO was given to rats given fructose, increased insulin and resistin levels decreased, while decreased adiponectin levels were increased. Conclusion: Fructose-induced impaired metabolic changes in brain tissue were partially ameliorated when EPO was administered. Accordingly, the use of EPO in the medical setting may be recommended by clinicians to reduce the harmful effects on the brain, since metabolic changes in the brains of rat fed with high fructose content can also occur with the intake of fructose from various foods in humans.

The study was conducted to investigate how Ferula rigidula extract affected sperm profile, antioxidant parameters, and stereological profile in experimental diabetic rats. Performed on forty-nine male rats. The rats were randomly assigned to control group, diabetic group, diabetic + Ferula rigidula group 1, diabetic + Ferula rigidula group 2, diabetic + glibenclamide group, Ferula rigidula group 1, and Ferula rigidula group 2. While sperm count, motility, antioxidant parameters, testosterone hormone, germinal epithelial volume, and germinal epithelial height decreased in the diabetic group, abnormal sperm count, malondialdehyde level, and lumen volume increased. When ferula rigidula (extract) was given to the diabetic rats, it brought the stereological findings to the same level as the control group. In particular, Ferula rigidula group 1 had improved testosterone levels and stereological findings when Ferula rigidula extract was administered alone. As a result, Ferula rigidula extract has an antioxidant role and can be used to alleviate the problems caused by diabetes in the male reproductive system.

Yapılan çalışmada acıbadem (Amygdalus nana L.) ve tatlı badem (Amygdalus trichamygdalus) ekstraktlarının antimikrobiyal etkisi araştırılmıştır. Diyarbakır Ergani ilçesinden toplanan tatlı badem ve Van Tuşba ilçesinden toplanan acı badem bitkilerinin ekstraktlarının deiyonize su, alkol ve eter içerisinde çözünmesi sağlanmıştır. Çalışmada patojen olarak, maya mantarı, gram pozitif ve gram negatif bazı bakteriler kullanılmıştır. Ekstraktların patojenler üzerine etkileri disk difüzyon metodu kullanılarak belirlenmiştir. Badem ekstraktlarının bakterilere karşı oluşturduğu zonlar göz önüne alındığında Amygdalus nana L. (Acı badem) bitkisininden elde edilen ekstraktın gösterdiği en yüksek inhibitör etkinin Enterococcus faecalis’e karşı olduğu belirlenmiştir. Amygdalus trichamygdalus (Tatlı Badem) bitkisinden elde edilen ekstraktın gösterdiği en yüksek inhibitör etkinin Staphylococcus aureus ve Escherichia coli bakterilerine karşı olduğu görülmüştür.