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    Behavioral and Cognitive Consequences of Obesity in Parents and Offspring in Female and Male Rats: Implications of Neuroinflammation and Neuromodulation
    (Springer, 2022) Demir, Enver Ahmet; Gulbol-Duran, Gulay; Urhan-Kucuk, Meral; Dogan, Hatice; Tutuk, Okan; Cimen, Funda; Bayirli, Mucella
    Obesity is a rapidly growing public health concern that can create a family-wise burden. This study was aimed to investigate behavioral, cognitive, neuroinflammatory, and neuromodulatory consequences of the diet and parental obesity. Female and male Wistar albino rats were fed on either an obesogenic or standard diet for 12 weeks, beginning with weaning. Thereafter, the animals were matched and allowed to mate. Pups born to obese or normal parents received either the diet or standard chow to the same age. The obesogenic diet and/or parental obesity increased the locomotor activity in both females and males. The diet exhibited anxiolytic-like and antidepressant-like properties, and impaired short-term object memory as well as spatial memory. Interestingly, the obesogenic diet resulted in neuroinflammation only in naive animals, but not in the ones with parental obesity. BDNF, SIRT1, and p53 expressions were decreased, whereas RelN expression was increased in the brain with the diet, regardless of parental obesity. Multi-factor analyses demonstrated that the obesogenic diet is the prominent influencer of cognitive, neuroinflammatory, and neuromodulatory results while parental obesity has an effect on spatial memory, neuroinflammation, and hippocampal RelN and p53 expressions. Here, we provided supporting evidence for detrimental cognitive and neuroinflammatory consequences of early life consumption of the obesogenic diet which accompanies alterations in neuromodulatory factors. Surprisingly, the diet was found beneficial against anxiety-like and depression-like behaviors, and additionally, parental obesity was demonstrated to impair some aspects of cognitive performance which appears unrelated to neuroinflammation.
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    Effects of Interactions among Gene Polymorphisms of the Renin-Angiotensin-Aldosterone System on Hypertension in Turkish People from Southeast Anatolia
    (Sciendo, 2019) Arpaci, Abdullah; Urhan-Kucuk, Meral; Bayramoglu, Aysegul; Guler, Halil Ibrahim; Ecevit, Hasret; Suner, Arif; Karakas-Celik, Sevim
    Introduction: Hypertension (HT) is characterized by high blood pressure. The reninangiotensin-aldosterone system (RAAS) plays a crucial role in blood pressure (BP) regulation by maintaining vascular tone and the water-sodium balance. We aimed to investigate whether there is any relation between AGT (M235T), ACE (I/D), and AGTR1 (A1166C) genetic polymorphisms and hypertension among Turkish people from Southeast Anatolia. Method and Results: A total of 210 individuals, consisting of 102 healthy controls and 108 patients with essential hypertension admitted to the Cardiology Department of the Adiyaman University Research and Application Hospital were included the study. DNA isolation was performed from the blood samples via commercial kit. Genotype determination was determined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Statistically significant differences were found between the control and patient groups in terms of genotype distribution and allelic frequencies of ACE I/D polymorphisms. Significant differences were found in the frequencies of ICM, DCM, DCT, DAT between the patient and control groups. Conclusions: In this study, we found a significant association of ACE I/D polymorphism with HT, and we showed that the I allele can increase the risk of HT in Turkish people from Southeast Anatolia. Although we did not find any association between independent AGT M235T and AGT1R A1166C polymorphisms and HT, we observed that the DCM, DCT, and DAT haplotypes of ACE/AGT1R/AGT polymorphisms reduced the risk of hypertension, while the ICM haplotype increased it.
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    Öğe
    The Role of Oxidative Stress in Apoptosis and Cell Proliferation of Human Bronchial Epithelial Cells
    (Pleiades Publishing Inc, 2021) Ecevit, Hasret; Urhan-Kucuk, Meral; Uluca, Haluk; Tap, Duygu; Arpaci, Abdullah
    Oxidative stress is an important pathophysiological factor in chronic respiratory diseases. Our study aimed at elucidating through which pathway oxidative stress-mediated apoptosis occurs at the gene expression level under oxidative stress in the human bronchial epithelial cell line BEAS-2B. Suitable doses and time period were detected by exposing BEAS-2B cells to hydrogen peroxide (H2O2) at different doses and time periods, and the oxidative-damaged cell culture model was designed. The treatment and control groups were compared in terms of gene expression levels determined by Quantitative Real Time Polymerase Chain Reaction. The oxidative-damaged cell model was confirmed by the spectrophotometric measurement of malondialdehyde and catalase activity (p < 0.05). Caspase-3, caspase-9, bax, and bak gene expression levels increased significantly in the treatment groups compared to the control group (p < 0.05). There were not any significant differences between the groups in terms of caspase-8, Bcl-2, and bik (p > 0.05). p53 and p21 gene expression levels were found to be significantly higher in the treatment groups (p < 0.05). H2O2-induced oxidative stress, induced apoptosis through the intrinsic pathway at gene expression level in the bronchial epithelial BEAS-2B cells was observed.