2 results
Search Results
Now showing 1 - 2 of 2
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 - Scopus: 2In-Vivo Antioxidant and Therapeutic Effects of Ellagic Acid on Ischemia-Reperfusion Injury in Skeletal Muscle(Turkish National Vascular and Endovascular Surgery Society, 2025) Demirtas, H.; Ozer, A.; Yigit, D.; Dursun, A.D.; Yigman, Z.; Kosa, C.; Arslan, M.Aim: Skeletal muscle ischemia-reperfusion (IR) injury is a critical clinical issue characterized by oxidative stress, inflammation, and tissue damage, potentially leading to systemic organ dysfunction. Ellagic acid (EA), a naturally occurring polyphenolic compound, is widely recognized for its strong antioxidative, anti-inflammatory, and antiapoptotic effects demonstrated in various preclinical studies. This study sought to assess the therapeutic effects of EA in a rat model of lower extremity IR injury, focusing on histopathological and biochemical parameters. Material and Methods: 24 male Albino Wistar rats were randomly divided into four groups: Sham, EA, IR, and IR+EA. IR injury was induced by occluding the infrarenal abdominal aorta for 45 minutes, followed by 120 minutes of reperfusion. EA (40 mg/kg) was administered intraperitoneally prior to reperfusion. Left gastrocnemius muscle samples were collected for histopathological and biochemical analyses, including TOS, TAS, OSI, levels and PON-1 enzyme activity. Results: The IR group showed marked muscle injury, with a significantly higher total injury score (10.00±0.63) compared to the Sham (2.00±0.58) and EA groups (2.00±0.52) (p<0.001, both). The IR-EA group demonstrated notable improvement, with a reduced total injury score (6.17±0.54), which was also significantly lower than the IR group (p<0.001). Biochemically, TAS levels and PON-1 activity significantly decreased while TOS and OSI levels increased in the IR group compared to the sham and EA groups. In addition, EA treatment significantly increased TAS levels and PON-1 activity while reducing TOS and OSI levels in the IR-EA group compared to the IR group (p=0.039, p=0.045, p=0.045, p=0.007, respectively). Conclusion: EA effectively mitigated skeletal muscle damage induced by IR injury through its antioxidative, anti-inflammatory, and antiapoptotic mechanisms. The results suggest that EA exhibits potential effects as a therapeutic agent in managing IR-related injuries. © 2025, Turkish National Vascular and Endovascular Surgery Society. All rights reserved.
