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Showing papers by "Göksel Şener published in 2018"


Journal ArticleDOI
TL;DR: RF exerts both the antioxidant and anti‐inflammatory effects against AA‐induced colonic inflammation by suppressing neutrophil accumulation, inhibiting reactive oxidant generation, preserving endogenous glutathione, improving oxidative DNA damage and regulating inflammatory mediators, suggesting a future potential role in the treatment and prevention of ulcerative colitis.
Abstract: Riboflavin (RF) has been found to be a promising antioxidant and/or anti-inflammatory agent in several studies. However, the effect of RF against acetic acid (AA)-induced colonic injury is currently unknown. This study aimed to investigate the potential antioxidant and protective effects of RF in a rat model of ulcerative colitis. Starting immediately after the colitis induction (AA+RF group) or 1 week before the colitis induction (RF+AA+RF group), the rats were treated with RF (25 mg/kg per day; p.o.) for 3 days. The control and AA groups received saline (1 mL; p.o.) whereas AA+SS group (positive control) received sulfasalazine (100 mg/kg per day; p.o.) for 3 days. Colonic samples were taken for the biochemical and histological assessments on the third day. High damage scores, elevated tissue wet weight index (WI), tissue myeloperoxidase (MPO) activity, 8-hydroxy-2'-deoxyguanosine levels and chemiluminescence values, and a pronounced decrease in antioxidant glutathione (GSH) levels of the AA group were all reversed by RF pretreatment (RF+AA+RF group) and SS treatment (AA+SS group) (P < .05-.001). Tissue WI, MPO activity and GSH levels were not statistically changed in the AA+RF group. Western blot analysis revealed that the decreased protein expressions of tissue collagen (COL) 1A1, COL3A1 and transforming growth factor-β1 in the AA group were elevated in all the treatment groups (P < .05-.001). In conclusion, RF exerts both the antioxidant and anti-inflammatory effects against AA-induced colonic inflammation by suppressing neutrophil accumulation, inhibiting reactive oxidant generation, preserving endogenous glutathione, improving oxidative DNA damage and regulating inflammatory mediators, suggesting a future potential role in the treatment and prevention of ulcerative colitis.

19 citations


Journal ArticleDOI
TL;DR: The effects of melatonin treatment with or without insulin were examined in diabetic rat brain in order to investigate the role of oxidative stress in the development of diabetic complications.
Abstract: Background Diabetes mellitus is an endocrine disorder which is characterized by the development of resistance to the cellular activity of insulin or inadequate insulin production. It leads to hyperglycemia, prolonged inflammation, and oxidative stress. Oxidative stress is assumed to play an important role in the development of diabetic complications. Melatonin is the hormone that interacts with insulin in diabetes. Therefore, in this study, the effects of melatonin treatment with or without insulin were examined in diabetic rat brain. Methods Rats were divided into five groups as control, diabetes, diabetes + insulin, diabetes + melatonin, and diabetes + melatonin + insulin. Experimental diabetes was induced by streptozotocin (60 mg/kg, i.p.). Twelve weeks after diabetes induction, rats were decapitated. Malondialdehyde, glutathione, sialic acid and nitric oxide levels, superoxide dismutase, catalase, glutathione-S-transferase, myeloperoxidase, and tissue factor activities were determined in brain tissue. Results Melatonin alone showed its antioxidant effect by increasing brain glutathione level, superoxide dismutase, catalase, and glutathione-S-transferase activities and decreasing malondialdehyde level in experimental diabetes. Although insulin did not have a significant effect on glutathione and glutathione-S-transferase, its effects on lipid peroxidation, superoxide dismutase, and catalase were similar to melatonin; insulin also decreased myolopeoxidase activity and increased tissue factor activity. Combined melatonin and insulin treatment mimicked the effects of insulin. Conclusion Addition of melatonin to the insulin treatment did not change the effects of insulin, but the detailed role of melatonin alone in the treatment of diabetes merits further experimental and clinical investigation.

16 citations


Journal ArticleDOI
TL;DR: The effects of resveratrol, an antioxidant, on post-RT ED preserved the metabolic pathways involved in erectile function and provided functional protection.
Abstract: Radiotherapy (RT) for prostate cancer (PC) can cause erectile dysfunction (ED) by damaging neurovascular structures with oxidative stress. In this study, we evaluated the effects of resveratrol, an antioxidant, on post-RT ED. Fifty rats in five groups were evaluated; control (C), prostate-confined radiotherapy with short- and long-term vehicle or resveratrol treatment. Cavernosal tissues were obtained to analyze glutathione (GSH), nitric oxide (NO), cyclic guanosine monophosphate (cGMP), 8-hydroxy-2′-deoxy-guanosine (8-OHdG) levels and superoxide dismutase (SOD), caspase-3 activities, sirtuin-1, Foxo-3, nNOS, and eNOS protein expressions. Intracavernosal pressures (ICP) were measured for the long-term treatment group. In the RT + long-term vehicle treatment group, tissue GSH, NO, cGMP, and SOD activity were decreased while 8-OHdg levels and caspase-3 activities were increased. Radiotherapy caused a decrease in sirtuin-1, nNOS, and eNOS protein expressions. These parameters were reversed by resveratrol treatment. Foxo-3 protein expressions were unaltered in the RT + short-term vehicle treatment group and started to increase as a defense mechanism in the RT + long-term vehicle group; however, resveratrol treatment caused a significant increase in Foxo-3 expressions. Resveratrol preserved the metabolic pathways involved in erectile function and provided functional protection. Resveratrol can be used as a supplementary agent in patients undergoing radiotherapy to preserve erectile function.

16 citations


Journal ArticleDOI
TL;DR: This study aimed to evaluate the effects of platelet‐rich plasma (PRP) on a urethral injury (UI) model of male rats and found that PRP significantly reduces the likelihood of Urethral stricture in males.
Abstract: Aims Urethral stricture (US) formation is caused by fibrosis after excessive collagen formation following an injury or trauma to the urethra. In this study, we aimed to evaluate the effects of platelet-rich plasma (PRP) on a urethral injury (UI) model of male rats. Methods A UI model was used by applying a coagulation current to the urethras of male rats. There were four groups with six rats in each: control group, PRP applied to naive urethra, UI group, and UI with PRP application. PRP was applied to the urethra after a coagulation current-induced injury as soon as possible. On the 14th day, all rats were sacrificed and urethral tissues were investigated for collagen type I, collagen type III, platelet-derived growth factor-α, platelet-derived growth factor-β, and transforming growth factor-β using quantitative real-time polymerase chain reaction and Western blot analysis. The effect of urethral damage and healing was evaluated for collagen type I-to-collagen type III ratio. Results The collagen type I-to-collagen type III ratio was significantly higher in UI group (P 0.05). Conclusions The results of this study show that PRP has a preventive effect on stricture formation in a UI model of rats, as shown by its effect on collagen synthesis. Further studies that eventually show the effects of PRP on human tissues are necessary and promising.

14 citations


Journal ArticleDOI
TL;DR: The preventive effect of this powerful antioxidant can be attributed to its ability to balance oxidant‐antioxidant status, inhibit neutrophil infiltration, and regulate inflammatory mediators, suggesting a future role in the treatment and prevention of abdominal aortic aneurysms.

13 citations


Journal ArticleDOI
TL;DR: Montelukast attenuates bleomycin-induced inflammatory and oxidative lung injury and prevents lung collagen deposition and fibrotic response and might be regarded as new therapeutic agents for idiopathic pulmonary fibrosis.
Abstract: Background This study aims to investigate the early- and late-term effects of pharmacological inhibition of cysteinyl leukotriene activity by using montelukast in bleomycin-induced inflammatory and oxidative lung injury in an animal model. Methods The study included 48 male Wistar albino rats (weighing 250 g to 300 g). Rats were administered intratracheal bleomycin or saline and assigned into groups to receive montelukast or saline. Bronchoalveolar lavage fluid and lung tissue samples were collected four and 15 days after bleomycin administration. Results Bleomycin resulted in significant increases in tumor necrosis factor-alpha levels (4.0±1.4 pg/mL in controls vs. 44.1±14.5 pg/mL in early-term vs. 30.3±5.7 pg/mL in late-term, p<0.001 and p<0.001, respectively), transforming growth factor beta 1 levels (28.6±6.6 pg/mL vs. 82.3±14.1 pg/mL in early-term vs. 60.1±2.9 pg/mL in late-term, p<0.001 and p<0.001, respectively), and fibrosis score (1.85±0.89 in early-term vs. 5.60±1.14 in late-term, p<0.001 and p<0.01, respectively). In bleomycin exposed rats, collagen content increased only in the late-term (15.3±3.0 ?g/mg in controls vs. 29.6±9.1 ?g/mg in late-term, p<0.001). Montelukast treatment reversed all these biochemical indices as well as histopathological alterations induced by bleomycin. Conclusion Montelukast attenuates bleomycin-induced inflammatory and oxidative lung injury and prevents lung collagen deposition and fibrotic response. Thus, cysteinyl leukotriene receptor antagonists might be regarded as new therapeutic agents for idiopathic pulmonary fibrosis.

9 citations


Journal ArticleDOI
TL;DR: Rb exerted anti-oxidative and anti-inflammatory effects on CNI in a CNI rat model and can be a potential beneficial agent to improve erectile function in nerve-sparing radical prostatectomy patients as a preemptive penile rehabilitation strategy, although further clinical studies are needed.
Abstract: effects of riboflavin (Rb) on bilateral CNI in a rat model. Materials and Methods: Twenty-four male rats were divided into four groups: control (C), patients with bilateral CNI, those with CNI receiving postoperative Rb treatment (CNI+Rb), and those with CNI receiving preand post-operative Rb treatment (Rb+CNI+Rb). Bilateral CNI was performed in all groups except for C. The CNI+Rb group was treated with 30 mg/kg Rb daily after CNI for two weeks; the Rb+CNI+Rb group was treated with 30 mg/kg Rb daily one week before CNI and then for two weeks after injury. Mean arterial pressure (MAP) and intracavernosal pressure (ICP) were measured 14 days after CNI in all groups. Tissue malondialdehyde, cyclic guanosine monophosphate, nerve growth factor, superoxide dismutase and total nitric oxide synthase (NOS) activities, neuronal NOS (nNOS) and inducible NOS (iNOS) were analyzed. Results: ICP/MAP ratio was significantly lower in the CNI (p<0.01) and CNI+Rb groups (p<0.05) compared to the control group, however, the Rb+CNI+Rb group had results comparable to the C group in terms of nNOS and iNOS expression in the Western Blot analysis. Conclusion: Rb exerted anti-oxidative and anti-inflammatory effects on CNI in a CNI rat model. Rb can be a potential beneficial agent to improve erectile function in nerve-sparing radical prostatectomy patients as a preemptive penile rehabilitation strategy, although further clinical studies are needed.