Dursun, Ali Doğan
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Dursun, Ali D. D.
D. Dursun
D.,Ali Dogan
Dursun A.
A., Dursun
Dursun, Ali
Ali Doan
Dursun, Ali Dogan
Dursun, A. D.
A.,Dursun
Dursun,A.D.
D., Ali Doğan
Dursun, Ali Doğan
D.,Ali Doğan
A.D.Dursun
Ali Doğan, Dursun
A. D. Dursun
Dursun, Ali D.
Ali Dogan, Dursun
D., Ali Dogan
D. Dursun
D.,Ali Dogan
Dursun A.
A., Dursun
Dursun, Ali
Ali Doan
Dursun, Ali Dogan
Dursun, A. D.
A.,Dursun
Dursun,A.D.
D., Ali Doğan
Dursun, Ali Doğan
D.,Ali Doğan
A.D.Dursun
Ali Doğan, Dursun
A. D. Dursun
Dursun, Ali D.
Ali Dogan, Dursun
D., Ali Dogan
Job Title
Doçent Doktor
Email Address
ali.dursun@atilim.edu.tr
Main Affiliation
Basic Sciences
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WoS Researcher ID
Sustainable Development Goals
1NO POVERTY
0
Research Products
2ZERO HUNGER
0
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3GOOD HEALTH AND WELL-BEING
21
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4QUALITY EDUCATION
0
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5GENDER EQUALITY
1
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6CLEAN WATER AND SANITATION
2
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7AFFORDABLE AND CLEAN ENERGY
1
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8DECENT WORK AND ECONOMIC GROWTH
0
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9INDUSTRY, INNOVATION AND INFRASTRUCTURE
1
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10REDUCED INEQUALITIES
0
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11SUSTAINABLE CITIES AND COMMUNITIES
1
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12RESPONSIBLE CONSUMPTION AND PRODUCTION
0
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13CLIMATE ACTION
0
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14LIFE BELOW WATER
2
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15LIFE ON LAND
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16PEACE, JUSTICE AND STRONG INSTITUTIONS
1
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17PARTNERSHIPS FOR THE GOALS
0
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Documents
71
Citations
550

Scholarly Output
50
Articles
47
Views / Downloads
143/55
Supervised MSc Theses
1
Supervised PhD Theses
0
WoS Citation Count
282
Scopus Citation Count
302
Patents
0
Projects
0
WoS Citations per Publication
5.64
Scopus Citations per Publication
6.04
Open Access Source
31
Supervised Theses
1
| Journal | Count |
|---|---|
| International Journal of General Medicine | 4 |
| Drug Design, Development and Therapy | 4 |
| Medicina | 3 |
| Talanta | 2 |
| Journal of Updates in Cardiovascular Medicine | 2 |
Current Page: 1 / 7
Scopus Quartile Distribution
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4 results
Scholarly Output Search Results
Now showing 1 - 4 of 4
Article Citation - Scopus: 1Protective Role of Bromelain’s Antioxidant and Anti-Inflammatory Effects in Experimental Lower Limb Ischemia-Reperfusion Injury(Nature Portfolio, 2025) Sezen, Saban Cem; Demirtas, Huseyin; Yildirim, Alperen Kutay; Ozer, Abdullah; Dursun, Ali Dogan; Kucuk, Aysegul; Arslan, Mustafa; Ozalp, Veli Cengiz; Kucuk, Işın GunesIschemia-reperfusion (IR) injury is a multifaceted pathological process characterized by excessive oxidative stress and inflammatory responses upon restoration of blood flow. Bromelain, a proteolytic enzyme complex derived from pineapple, exhibits robust antioxidant and anti-inflammatory activities. This study aimed to evaluate the protective effects and underlying mechanisms of bromelain on oxidative stress and inflammation in an experimental rat model of lower limb ischemia-reperfusion injury. Twenty-four male Wistar Albino rats were randomly allocated into four groups: Sham-operated control (SHAM), Bromelain-only (BR), Ischemia-Reperfusion (IR), and Ischemia-Reperfusion with Bromelain treatment (IR + BR). Bromelain (40 mg/kg) was administered intraperitoneally before ischemia induction. The IR model involved 45 min of infrarenal abdominal aorta occlusion followed by 120 min of reperfusion. Oxidative biomarkers (total antioxidant status [TAS], total oxidant status [TOS], oxidative stress index [OSI]) and histopathological parameters (muscle atrophy, degeneration, leukocyte infiltration, internalization of nuclei, fragmentation, and hyalinization) were analyzed. Significant increases in muscle degeneration, leukocyte infiltration, nuclear internalization, fragmentation, and elevated oxidative stress biomarkers (increased TOS and OSI, decreased TAS) were observed in the IR group compared to controls. Bromelain treatment (IR + BR) significantly ameliorated these effects, reducing muscle tissue damage, inflammation, and oxidative imbalance compared to the untreated IR group. Bromelain effectively mitigates lower limb ischemia-reperfusion injury by reducing oxidative stress, restoring antioxidant capacity, and suppressing inflammatory responses. These protective effects suggest that bromelain holds potential as a therapeutic agent for managing oxidative and inflammatory damages associated with IR conditions, warranting further clinical investigation.Article Citation - Scopus: 3Protective Effects of Metformin in Non-Diabetic Rats With Experimentally Induced Lower Extremity Ischemia-Reperfusion Injury(Turkish National Vascular and Endovascular Surgery Society, 2025) Küçük, Ayşegül; Dursun, Alı Dogan; Arslan, Mustafa; Sezen, Şaban Cem; Yıldırım, Alperen Kutay; Özer, Abdullah; Demirtas, HuseyinAim: Lower extremity ischemia-reperfusion (IR) injury can lead to substantial skeletal muscle damage and systemic complications, primarily driven by oxidative stress and inflammation. In addition to its well-known glucose-lowering effects, metformin possesses antioxidant and anti-inflammatory properties that may confer protection against tissue damage caused by IR. This study aims to evaluate the potential protective effects of metformin on skeletal muscle injury using a rat model of lower extremity IR.Material and Methods: A total of twenty-four male Wistar albino rats were randomly divided into four experimental groups: Control (C), Ischemia-Reperfusion (IR), IR with metformin at 4 mg/kg (IR+M4), and IR with metformin at 8 mg/kg (IR+M8). Ischemia was induced by clamping the infrarenal aorta for 45 minutes, followed by a reperfusion period of 120 minutes. In the treatment groups, metformin was administered intraperitoneally at the onset of ischemia. Gastrocnemius muscle tissues were harvested for subsequent histopathological and biochemical evaluations, including measurements of Total Antioxidant Status (TAS), Total Oxidant Status (TOS), and Oxidative Stress Index (OSI).Results: Histopathological analysis demonstrated a significant reduction in muscle atrophy, degeneration, leukocyte infiltration, and fiber fragmentation in the IR+M8 group compared to the IR group. Biochemical assessments showed that TAS levels were considerably elevated, whereas TOS and OSI levels were markedly reduced in the metformin-treated groups, with the most prominent effects observed at the higher dosage of 8 mg/kg.Conclusion: The findings indicate that metformin exerts a dose-dependent protective effect against skeletal muscle injury resulting from lower extremity ischemia-reperfusion in rats. These protective properties are likely due to metformin’s antioxidant and anti-inflammatory mechanisms, highlighting its potential therapeutic value in mitigating IR-induced tissue damage.Article Citation - WoS: 8Ozone Administration Reduces Myocardial Ischemia Reperfusion Injury in Streptozotocin-Induced Diabetes Mellitus Rat Model(Baycinar Medical Publishing, 2024) Gulcan, M.B.; Demirtas, H.; Ozer, A.; Yıgman, Z.; Dursun, A.D.; Arslan, M.; Oktar, G.L.Objective: This study aimed to investigate the effects of ozone therapy on myocardial ischemia/reperfusion injury in a diabetic rat model. Methods: The experimental study included 38 male Wistar Albino rats weighing between 200 and 250 g. The rats were randomly assigned to five groups. The sham group included six rats, while the other groups had eight rats each. The other groups were the diabetic ozone group, the diabetic group, the diabetic ischemia/reperfusion group (DIR), and the diabetic ischemia/reperfusion ozone group (DIRO). A total of 32 rats received 65 mg/kg streptozotocin, and a week after the administration, diabetes was confirmed by measuring blood sugar. The rats were fed ad libitum for 40 days to reveal macrovascular complications of diabetes. Malondialdehyde, catalase, superoxide dismutase, paraoxonase-1, total oxidative status, total antioxidant status, and oxidative stress index were assessed. A TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assay was employed to assess apoptosis. Results: Histologic and biochemical assessments showed the benefits of ozone in myocardial ischemia/reperfusion injury in diabetic rats. The DIRO group was found to be superior to the DIR group. Conclusion: Ozone has cardioprotective effects in streptozotocin-induced diabetic rats through its antioxidant properties against oxidative stress. The study is unique in terms of ozone’s protective effects in diabetic rats against myocardial ischemia/reperfusion injury. However, further studies are needed to confirm our findings. © (2024), (Baycinar Medical Publishing). All rights reserved.Article Effects of Pomegranate Seed Oil on Lower Extremity Ischemia-Reperfusion Damage: Insights into Oxidative Stress, Inflammation, and Cell Death(MDPI, 2025) Bozok, Ummu Gulsen; Ergorun, Aydan Iremnur; Kucuk, Aysegul; Yigman, Zeynep; Dursun, Ali Dogan; Arslan, MustafaAim: This study sought to clarify the therapeutic benefits and mechanisms of action of pomegranate seed oil (PSO) in instances of ischemia–reperfusion (IR) damage in the lower extremities. Materials and Methods: The sample size was determined, then 32 rats were randomly allocated to four groups: Control (C), ischemia–reperfusion (IR), low-dose PSO (IR + LD, 0.15 mL/kg), and high-dose PSO (IR + HD, 0.30 mL/kg). The ischemia model in the IR group was established by occluding the infrarenal aorta for 120 min. Prior to reperfusion, PSO was delivered to the IR + LD and IR + HD groups at doses of 0.15 mL/kg and 0.30 mL/kg, respectively, followed by a 120 min reperfusion period. Subsequently, blood and tissue specimens were obtained. Statistical investigation was executed utilizing Statistical Package for the Social Sciences version 20.0 (SPSS, IBM Corp., Armonk, NY, USA). Results: Biochemical tests revealed significant variations in total antioxidant level (TAS), total oxidant level (TOS), and the oxidative stress index (OSI) across the groups (p < 0.0001). The IR group had elevated TOS and OSI levels, whereas PSO therapy resulted in a reduction in these values (p < 0.05). As opposed to the IR group, TASs were higher in the PSO-treated groups. Histopathological analysis demonstrated muscle fiber degeneration, interstitial edema, and the infiltration of cells associated with inflammation in the IR group, with analogous results noted in the PSO treatment groups. Immunohistochemical analysis revealed that the expressions of Tumor Necrosis Factor-alpha (TNF-α), Nuclear Factor kappa B (NF-κB), cytochrome C (CYT C), and caspase 3 (CASP3) were elevated in the IR group, while PSO treatment diminished these markers and attenuated inflammation and apoptosis (p < 0.05). The findings demonstrate that PSO has a dose-dependent impact on IR injury. Discussion: This research indicates that PSO has significant protective benefits against IR injury in the lower extremities. PSO mitigated tissue damage and maintained mitochondrial integrity by addressing oxidative stress, inflammation, and apoptotic pathways. Particularly, high-dose PSO yielded more substantial enhancements in these processes and exhibited outcomes most comparable to the control group in biochemical, histological, and immunohistochemical investigations. These findings underscore the potential of PSO as an efficacious natural treatment agent for IR injury. Nevertheless, additional research is required to articulate this definitively.

