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Öğe Effects of resveratrol on diabetes-induced vascular tissue damage and inflammation in male rats(Walter De Gruyter Gmbh, 2017) Pektaş, Ayhan; Pektaş, Mehmet Bilgehan; Koca, Halit Buğra; Tosun, Murat; Aslan, Esra; Koca, Selcan; Sadi, GökhanObjective: The present study aims to investigate the short-term effects of resveratrol on histopathological characteristics and inflammatory cytokines of the heart and thoracic aorta tissues in animal models of streptozotocin (STZ)-induced diabetes. Methods: Male Wistar rats were randomly divided into four groups; (1) control/vehicle, (2) control/20 mg/kg resveratrol, (3) diabetic/vehicle, (4) diabetic/20 mg/kg resveratrol. Heart and thoracic aorta were examined histopathologically and the levels of interleukin (IL)-1 beta, IL-18 and tissue necrosis factor (TNF)-alpha were analyzed by ELISA. Malondialdehyde (MDA) contents were determined with HPLC. Results: Diabetes group had significantly higher vascular MDA content (p < 0.05) as compared with the control and resveratrol treated groups. Resveratrol significantly reduced vascular MDA level in diabetic animals (p < 0.05). Significant elevation in IL-1 beta and TNF-alpha contents in thoracic aorta and IL-18 contents in cardiac and arterial tissues with diabetes were almost normalized with resveratrol treatment. Additionally, diabetic animals demonstrated significant endothelial damage, irregularities in smooth muscle fibers and degeneration of elastic fibers in thoracic aortas together with significant irregularities and hypertrophy in cardiac muscle fibers. Resveratrol significantly improved most of these histopathological alterations. Conclusion: Four-week-long intraperitoneal administration of resveratrol may restore the diabetes related inflammation and oxidative stress within the cardiovascular system.Öğe High-fructose in drinking water initiates activation of inflammatory cytokines and testicular degeneration in rat(Taylor & Francis Ltd, 2019) Yıldırım, Onur Gökhan; Sumlu, Esra; Aslan, Esra; Koca, Halit Buğra; Pektaş, Mehmet Bilgehan; Sadi, Gökhan; Akar, FatmaThe increased consumption of high-fructose in diet may contribute to high prevalence of metabolic syndrome in the world. The influence of high-fructose diet on male reproductive system has been poorly documented. In this study, we investigated the effects of dietary high-fructose on the expression of inflammatory cytokines in association with certain testicular proteins and sex hormones in the testis of rats. Fructose was given to the rats as 20% solution (7.8mg/kg) in drinking water for 15 weeks. Dietary high-fructose caused testicular degeneration, also decreased testicular concentration of testosterone and right testis absolute weight. This dietary intervention increased iNOS and TNF-alpha mRNAs as well as iNOS, NF-kappa B, and p-NF-kappa beta proteins, but decreased IL-10 and IL-6 mRNAs expressions, in testicular samples of rats. Moreover, testicular TNF-alpha, IL-1 beta, and iNOS and plasma IL-1 beta levels were significantly increased in rats fed with fructose. A marked increase in the expression level of IGF-1R protein was considered in testicular tissue of fructose-treated rats. The expression intensities of c-kit, claudin-1, and pan-cadherin were comparable in seminiferous tubules of control and fructose-treated rats. In conclusion, high-fructose intake of rats leads to activation of inflammatory cytokines, which is accompanied by testicular degeneration. These changes could be responsible for hormonal dysfunction with low intra-testicular testosterone level, which could be relevant to male infertility.Öğe İmpact of juglone, a pin1 inhibitor, on oral carcinogenesis induced by 4-nitroquinoline-1-oxide (4nqo) in rat model(Mdpi, 2024) Topal, Olgun; Topal, Burcu Güçyetmez; Bas, Yunus; Ongan, Bünyamin; Sadi, Gökhan; Aslan, Esra; Yavaş, Betül DemircilerBackground and Objectives: PIN1 is overexpressed in several human cancers, including prostate cancer, breast cancer, and oral squamous carcinomas. Juglone (J), derived from walnut, was reported to selectively inhibit PIN1 by modifying its sulfhydryl groups. In this study, the potential effects of juglone, also known as PIN1 inhibitor, on oral cancer and carcinogenesis were investigated at the molecular level. Materials and Methods: 4-Nitroquinoline N-oxide (4-NQO) was used to create an oral cancer model in animals. Wistar rats were divided into five groups: Control, NQO, Juglone, NQO+J, and NQO+J*. The control group received the basal diet and tap water throughout the experiment. The NQO group received 4-NQO for 8 weeks in drinking water only. The Juglone group was administered intraperitoneally in a juglone solution for 10 weeks (1 mg/kg/day). The NQO+J group received 4-NQO in drinking water for 8 weeks, starting 1 week after the cessation of 4-NQO treatment. They were then administered intraperitoneally in a juglone solution for 10 weeks. (1 mg/kg/day). NQO+J* group: received 4 NQO for 8 weeks in drinking water and administered intraperitoneally in a juglone solution for 10 weeks (1 mg/kg/day). They were sacrificed at the end of the 22-week experimental period. The tongue tissues of the rats were isolated after the experiment, morphological changes were investigated by histological examinations, and the molecular apoptotic process was investigated by rt-qPCR and western blot. Results: Histological results indicate that tumors are formed in the tongue tissue with 4-NQO, and juglone treatment largely corrects the epithelial changes that developed with 4-NQO. It has been determined that apoptotic factors p53, Bax, and caspases are induced by the effect of juglone, while antiapoptotic factors such as Bcl-2 are suppressed. However, it was observed that the positive effects were more pronounced in rats given juglone together with 4-NQO. Conclusions: The use of PIN1 inhibitors such as juglone in place of existing therapeutic approaches might be a promising and novel approach to the preservation and treatment of oral cancer and carcinogenesis. However, further research is required to investigate the practical application of such inhibitors.Öğe Kefir prevents adipose tissue growth through the induction of apoptotic elements in high-fructose corn syrup-fed rats(Inst Animal Reproduction & Food Research Polish Acad Scıences Olsztyn, 2023) Aslan, Esra; Sadi, Gökhan; Güzel, Hilal; Karaca, Çiğdem; Korkmaz, Ömer Adil; Pektaş, Mine K.Consumption of high-fructose corn syrup (HFCS) in the diet is a causal factor in the development of abdominal obesity; however, the molecular mechanism behind this association is still up for debate. This study evaluated the metabolic disturbances that are caused by HFCS on adipose tissue as well as the possibility of kefir as a therapy to prevent these metabolic disturbances. Male Wistar rats were divided into four groups: control, kefir, HFCS, and HFCS+kefir. HFCS (20%, w/v) was given in drinking water and kefir (1 mL/100 g body weight) by gastric gavage daily for 8 weeks. Levels of insulin signaling, inflammation, and apoptosis-associated proteins of adipose tissues were determined with Western blot and immunohistochemical techniques. Gene expressions were evaluated with semi-quantitative real-time polymerase chain reaction (qRT-PCR). The indirect terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) method was used to assess changes in apoptotic cells, and hematoxylin/eosin staining to determine adipocyte number and diameter. Accordingly, HFCS boosted protein kinase B (Akt) and p-Akt while reducing nuclear factor & kappa;B (NF-& kappa;B), and tumor necrosis factor alpha (TNF & alpha;) levels and kefir treatment restored Akt induction in HFCS-treated rats despite raising NF-& kappa;B, and TNF & alpha;. Increased expression of Akt and B-cell lymphoma-2 gene (Bcl2) was contrasted with decreased expression of Nfkb, Tnfa, tumor protein 53 gene (p53), and caspase-8 gene (Casp8). Furthermore, while there was a marked reduction in TUNEL-positive cells in the HFCS group, the number of such cells was greater in the HFCS+kefir group. These results show that HFCS intake suppresses apoptosis in adipose tissues, which may be responsible for tissue development and abdominal obesity and may be reversed with kefir administration due to the activation of apoptosis-associated genes and proteins.Öğe Kefir protects the liver against high fructose corn syrup induced phosphodiesterase hyperactivity(Walter De Gruyter GMBH, 2022) Pektaş, Mehmet Bilgehan; Aslan, Esra; Güzel, Hilal; Korkmaz, Ömer Adil; Çeleğen, Kübra; Sadi, GökhanObjectives Phosphodiesterases (PDEs) mediate several physiological activities, and alterations in PDE expressions might cause conflicts between functional and clinical effects. This study clarifies the eventual relationship between the hepatic insulin resistance-associated signaling elements and PDEs together with inflammatory markers and investigates the role of kefir in the treatment. Methods Male Wistar rats were grouped as Control, Kefir, HFCS (high-fructose corn syrup), and HFCS + Kefir. Daily HFCS (20% w/v) and kefir (1 mL/100 g weight) were given for 8-weeks. Hepatic expressions of PDE isoforms and insulin signaling elements were determined with qPCR and Western blot. The changes in hepatic phospholipase A2 (cPLA2) and insulin-like growth factor 1 receptor-alpha (IGF-1R alpha) were investigated histologically. Results HFCS upregulated hepatic PDEs while repressed primary insulin signaling elements at gene and protein levels. It also augmented cPLA2 and IGF-1R alpha expression. Kefir suppressed the PDEs and normalized the insulin signaling, and down-regulated cPLA2 and IGF-1R alpha in the liver of HFCS-fed rats. Conclusions The disruption of the insulin signaling pathway and activation of PDEs were negatively correlated in liver tissues of the HFCS-fed rats. Kefir treatment achieved a remarkable improvement in HFCS-dependent modifications, and it could be an excellent functional food against HFCS-induced insulin resistance, PDE hyperactivity, and inflammation.Öğe Mangiferin Induces Post-Implant Osteointegration in Male Diabetic Rats(Mdpi, 2024) Ongan, Bünyamin; Ekici, Ömer; Sadi, Gökhan; Aslan, Esra; Pektaş, Mehmet BilgehanBackground and Objectives: Hyperglycemia is known to undermine the osteointegration process of implants. In this study, the effects of mangiferin (MF) on the post-implant osteointegration process in a type-II diabetes model were investigated molecularly and morphologically. Materials and Methods: Sprague Dawley male rats were divided into three groups: control, diabetes, and diabetes + MF. All animals were implanted in their tibia bones on day 0. At the end of the 3-month experimental period, the animals' blood and the implant area were isolated. Biochemical measurements were performed on blood samples and micro-CT, qRT-PCR, histological, and immunohistochemical measurements were performed on tibia samples. Results: MF significantly improved the increased glucose, triglyceride-VLDL levels, and liver enzymes due to diabetes. By administering MF to diabetic rats, the osteointegration percentage and bone volume increased while porosity decreased. DKK1 and BMP-2 mRNA expressions and OPN, OCN, and OSN mRNA-protein expressions increased by MF administration in diabetic rats. Additionally, while osteoblast and osteoid surface areas increased with MF, osteoclast and eroded surface areas decreased. Conclusions: The findings of our study indicate that MF will be beneficial to the bone-repairing process and osteointegration, which are impaired by type-II diabetes.
