Scopus İndeksli Yayınlar Koleksiyonu
Permanent URI for this collectionhttps://hdl.handle.net/20.500.14627/7
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Article Citation - WoS: 4Citation - Scopus: 4Collagen Peptides and Saccharomyces Boulardii Cncm I-745 Attenuate Acetic Acid-Induced Colitis in Rats by Modulating Inflammation and Barrier Permeability(Wiley, 2025) Altinok, Oyku; Bas, Murat; Dolanbay, Elif Gelenli; Kolgazi, Meltem; Mert, Tugay; Uslu, Unal; Gelenli Dolanbay, ElifUlcerative colitis (UC) is an inflammatory bowel disease characterized by recurrent episodes of inflammation and tissue damage, with limited treatment options. This study aimed to investigate the effects of collagen peptides and Saccharomyces boulardii on acetic acid (AA)-induced colitis. Thirty-six male Sprague-Dawley rats were randomly divided into the following four groups: normal control (NC), colitis control (CC), collagen peptide (CP; 0.6 g/kg/day), and S. boulardii (SB; 250 mg/day). Colitis was induced by an intrarectal administration of AA in all groups except NC, and treatments were administered daily for 7 days. The therapeutic effects were evaluated by assessing the disease activity index (DAI), colon mass index, macroscopic and microscopic tissue damage, histopathological changes, zonula occludens (ZO)-1 protein expression, and myeloperoxidase (MPO) activity. The results showed that CP and SB treatments substantially alleviated DAI scores (p < 0.05) and reduced the colon mass index. Colon macroscopic and microscopic damages improved compared to the CC group (p < 0.01). Histologically, both treatments reduced inflammatory cell infiltration, crypt damage, and ulceration, with CP showing a slightly more pronounced effect. Immunohistochemical analysis revealed significant restoration of ZO-1 protein expression in the treated groups, indicating improvement in intestinal barrier integrity (p < 0.01). Furthermore, MPO activity was reduced in both CP and SB groups, significantly in the SB group (p < 0.01). These findings are consistent with previous studies that highlight the anti-inflammatory and barrier-enhancing effects of collagen peptides and probiotics in UC models.Article Exploring the Role of Adipose Tissue-Derived Hormones Asprosin and Leptin in the Onset of Depressive Symptoms in Newly Diagnosed Prediabetic Individuals(Elsevier B.V., 2025) Bahadir, F.E.; Demirel, O.U.; Yavuz, M.; Firat, O.; Yogurtcu, I.; Govdeli, Y.; Furuncuoglu, Y.Background: Type 2 diabetes and depression are common chronic conditions that often co-occur, likely driven by complex mechanisms that are not yet fully understood. Chronic low-grade inflammation may serve as a shared underlying factor in both conditions. This study aimed to determine whether adipose tissue-derived hormones asprosin and leptin, particularly asprosin, which is associated with inflammatory cytokines in glucose metabolism dysregulation and has not been studied in this context—might influence the onset of depressive symptoms. Methods: 112 participants were recruited from drug-naïve individuals. Blood samples were collected, anthropometric data recorded, the Beck Depression/Anxiety Inventories administered. Adapted questions assessed physical and social activity, as well as sleep habits, to account for environmental factors. After applying the exclusion criteria, participants were divided into prediabetic (n = 32) and normoglycemic groups (n = 30). Results: In the prediabetic group CRP was elevated (p < 0.001), with a positive correlation between asprosin and leptin (p < 0.001). Asprosin was positively correlated with TNF-α (p = 0.004), IL-6 (p = 0.002), and ESR (p < 0.001), and leptin with TNF-α (p = 0.008) and ESR (p = 0.018) but not with depressive symptoms or anxiety. Depressive symptoms were higher in prediabetic individuals with poor sleep quality. Conclusion: In groups with similar social and physical activity levels, poor sleep quality was associated with increased depressive symptoms. While asprosin and leptin correlated with higher inflammatory cytokines, they showed no significant association with depression, possibly due to the small sample size and early-stage evaluation. Larger studies are needed to confirm any potential link between these hormones and depression. © 2025 The AuthorsArticle Citation - Scopus: 4Dodder (Cuscuta Sp.) Extract Ameliorates Liver Fibrosis in Bile Duct-Ligated Rats(Istanbul University Press, 2022) Albayrak, O.; Ozbeyli, D.; Sen, A.; Cevik, O.; Erdogan, O.; Ercan, F.; Sener, G.; Ede-pazarbasi, SerenObjective: The aim is to examine the possible protective effect of Cuscuta sp. extract against liver damage induced by biliary obstruction in rats. Materials and Methods: To induce biliary obstruction, the bile duct ligation (BDL) method was used. Sprague Dawley rats were allocated to 4 groups: Control (C), Cuscuta (CUS), bile duct ligation (BDL), and bile duct ligation + Cuscuta (BDL+CUS). Control and BDL rats were given physiological saline (SF), while CUS and BDL+CUS groups were administered 250 mg/ kg of Cuscuta extract by oral gavage. At the end of 28th day, the rats were decapitated, serum and tissue samples were collected, and aspartate aminotransferase (AST), alanine transaminase (ALT), and direct and total bilirubin (DB and TB) levels were determined in blood samples. In liver tissues, transforming growth factor-β (TGF-β), 8-hydroxyguanosine (8-OHdG), hydroxyproline, and sodium-potassium ATPase (Na+/K+-ATPase) levels were determined. Results: Serum samples of rats with cholestasis had high ALT, AST, DB, and TB levels, while TGF-β, 8-OHdG, and hydroxyproline concentrations were found to be significantly high in tissues. Hepatic Na+/K+-ATPase levels were decreased through biliary obstruction. Biochemical parameters were drastically reversed by Cuscuta care; also, this was supported histologically. Conclusion: Results showed that Cuscuta extract, through its antioxidant and anti-inflammatory properties, provided protection against oxidative injury by biliary obstruction. Also, these results confirm the traditional use of Cuscuta sp. as hepatoprotective. © Ankara Medical Journal.All rights reserved.Article Citation - Scopus: 6Myrtus Communis L. Extract Ameliorates High Fat Diet Induced Kidney and Bladder Damage by Inhibiting Oxidative Stress and Inflammation(Istanbul University Press, 2022) Mustafaoglu, F.K.; Ertas, B.; Sen, A.; Akakin, D.; Sener, G.; Ercan, F.Objective: Obesity is associated with many diseases, including urinary system disorders such as chronic kidney disease and overactive bladder syndrome. Myrtus communis L. (MC) extract has been reported to have antioxidant and anti-inflammatory effects. The aim of this study was to investigate the protective effects of MC extract on high-fat diet (HFD)-induced kidney and bladder damage. Materials and Methods: Wistar albino male rats were divided into three experimental groups: control, HFD and HFD+MC. Experimental groups were fed a standard diet (control group) or HFD (HFD and HFD+MC groups) for 16 weeks. MC extract (100 mg/kg) was administered to the HFD+MC group orally during the last 4 weeks (5 days/week) of the experiment. High-density lipoprotein, total cholesterol, triglyceride and leptin levels were measured in blood serum. Tissue malondialdehyde (MDA), glutathione (GSH), 8-hydroxy-2'-deoxyguanosine (8-OHdG) and myeloperoxidase (MPO) levels were evaluated biochemically. Kidney and bladder morphology, NADPH oxidase-2 (NOX-2) and nuclear factor-kappa B (NF-ҡB)-positive and apoptotic cells were evaluated histologically. Results: Lipid profiles altered and leptin levels increased in blood serum. MDA, 8-OHdG and MPO levels increased and GSH level decreased in kidney and bladder in the HFD group. Moreover, degenerated kidney and bladder morphology, increased NOX-2 and NF-ҡB-positive and apoptotic cells were observed in this group. All of these biochemical and histological parameters were ameliorated in the HFD+MC group. Conclusion: HFD-induced obesity causes kidney and bladder damage by oxidative and inflammatory processes. MC extract may reduce oxidative stress and inflammation and play a protective role in obesity-related kidney and bladder damage. © 2022 by the Author(s).