WoS İndeksli Yayınlar Koleksiyonu
Permanent URI for this collectionhttps://hdl.handle.net/20.500.14627/6
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Article NADPH Oxidase-2 Inhibitor Apocynin Attenuates High-Fat Diet-Induced Kidney and Bladder Injury(Marmara Univ, Fac Medicine, 2025) Kanpalta Mustafaoglu, Fatma; Ertas, Busra; Sener, Goksel; Ercan, FerihaObjective: This study aimed to evaluate the effects of NADPH oxidase-2 (NOX-2) inhibitor apocynin (APC) on high-fat diet (HFD)induced renal and bladder injury. Materials and Methods: Wistar albino rats were divided into 4 groups: Control, HFD, HFD+dimetyl sulfoxide (DMSO), and HFD+APC. Rats in HFD, HFD+DMSO, and HFD+APC groups were fed with HFD for sixteen weeks. In the last 4 weeks of the experiment, either DMSO or APC (25 mg/kg, dissolved in DMSO) was applied to the HFD+DMSO or HFD+APC groups. Lipid profiles and leptin values were measured in blood serum. Renal and bladder oxidant/antioxidant parameters, histological changes in the tissues, NOX-2-, nuclear factor kappa B (NF-& kgreen;B)-immunopositive and apoptotic cells were evaluated. Results: At the end of the experiment, leptin, cholesterol, and triglyceride levels were higher and high-density lipoprotein levels were lower in the HFD and HFD+DMSO groups compared to controls. In these experimental groups, an increase in malondialdehyde, 8-hydroxy-deoxyguanosine and myeloperoxidase levels and a decrease in glutathione levels, as well as an increase in collagen, NOX-2-and NF & kgreen;-B-immunopositive and apoptotic cells were found. Also, a deterioration in kidney and bladder morphology was observed. All these biochemical and histopathological findings improved in the HFD+APC group. Conclusion: High-fed diet causes renal and bladder injury by increasing NOX-2 activity and inflammation via oxidative stress. APC might alleviate tissue injury by inhibiting oxidative stress.Article Citation - WoS: 1Citation - Scopus: 2Apocynin Exhibits an Ameliorative Effect on Endothelial Dysfunction/ Atherosclerosis-Related Factors in High-Fat Diet-Induced Obesity in Rats(Marmara Univ, Fac Medicine, 2024) Ayci, Nurdan Bulbul; Ertas, Busra; Kaya, Rumeysa Keles; Sevinc, Sevgi Kocyigit; Amuran, Gokce Gullu; Ercan, Feriha; Cetinel, Sule; Keles Kaya, Rumeysa; Bulbul Ayci, Nurdan; Kocyigit Sevinc, SevgiObjective: The aim of this study was to reveal the effect of apocynin (APO) on the factors involved in obesity-related endothelial dysfunction (ED) and atherosclerosis (AS). Materials and Methods: Male Wistar albino rats were divided into control (CNT), high-fat diet (HFD) and HFD+APO groups. HFD and HFD+APO groups were fed HFD for sixteen weeks. APO (25 mg/kg) was administered to the HFD+APO group for the last four weeks. The effects of APO on: AS-related metabolic parameters (triglyceride, total cholesterol, high-density lipoprotein-cholesterol, insulin and leptin), oxidative stress (OS), [ malondialdehyde, glutathione, nicotinamide adenine dinucleotide phosphate (NADPH)oxidase-2, oxidised-low-density lipoprotein (ox-LDL) and 8-hydroxy-2-deoxyguanosine], low-density lipoprotein and ox-LDL uptake potential (activin receptor-like kinase-1 and lectin-like oxidized low-density lipoprotein receptor-1, respectively), tissue inflammation inducible-nitric oxide synthase, nitric oxide), programmed cell death (terminal deoxynucleotidyl-transferase-dUTP-nick-end (alpha-smooth muscle actin), histology and ultrastructure of thoracic aorta were evaluated. Results: In obesity, APO had an ameliorative effect on metabolic parameters, OS, inflammation, ED, programmed cell death and oxLDL uptake potential, but not on foam cell formation and LDL uptake potential. Conclusion: Apocynin may improve ED and AS in obesity by suppressing OS-linked factors involved in the early stage of AS.Article Citation - WoS: 6Citation - Scopus: 6<i>beta Vulgaris</I> L. Var. Cicla Improves Memory Deficits in Intracerebroventricular Streptozotocin Injected Rats: Role on Neuroinflammation(Marmara Univ, 2021) Ertas, Busra; Topal, Fadime; Gulhan, Rezzan; Yanardag, Refiye; Sacan, Ozlem; Sener, Goksel; Aker, Rezzan GulhanAlzheimer's disease is a challenging disease for patients due to progressive loss of cognition and behavioral disorders. Disruption of cholinergic transmission and neuroinflammation are the most important mechanisms underlying cognitive damage. Beta vulgaris L. var. cicla (BV) has been reported to have various pharmacological effects associated with its rich antioxidant content. In addition, anti-cholinesterase and antiinflammatory activities of BV have been demonstrated in vitro. The aim of this study is to elucidate the therapeutic effect of BV against cognitive impairment, reduction in cholinergic transmission and neuroinflammation caused by intracerebroventricular (ICV) administration of streptozotocin (STZ). STZ was administered bilaterally at a dose of 3 mg/kg via ICV to rats, and BV treatment at a dose of 2 g/kg for 21 days was administered orally to STZ-induced animals. After behavioral tests, AChE activity, TNF-alpha and IL-1 beta levels were measured in hippocampus and cortex tissues excised from decapitated animals. Novel object recognition and passive avoidance test showed that the treatment of BV reverted the ICV-STZ induced memory dysfunctions in rats. Furthermore, increased AChE levels in the hippocampal and cortical tissues of STZ-induced rats were significantly reduced with 21 days of BV treatment. In conclusion, these results confirm that STZ administration caused cholinergic hypofunction, neuronal inflammation and cognitive dysfunction in rats, and BV therapy significantly inhibited these changes with its potential neuroprotective activity.