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Showing 2 results for Apoptosis

A. Shiroo, S. Salami, M. Khadem Ansari, F. Ghaderi Pakdel, K. Khadem Vatani, R. Saadatian, M. Karimipour,
Volume 10, Issue 1 (5-2008)
Abstract

Abstract Introduction: The purpose of this study was to determine and to assess the protective effect of vitamin E on cardiomyocyte apoptosis and oxidative stress status in the heart under hyperglycemic conditions, in vivo. Materias and Methods: Wistar male rats (n=16) at 6 months of age were made hyperglycemic by STZ. Same age, normal wistar rats (n=8) were used for comparison (controls). Diabetic rats were divided into two groups, the nontreated and those treated with vitamin E (300mg/kg/daily). Results: Diabetic rats exhibited severe apoptosis in cardiomyocytes. Also significant increases in lipid peroxidation as measured by 8- isoprostan, protein oxidation as measured by protein carbonyl content and superoxide dismutase were observed after 6 weeks. Catalase activity was shown to increase in controls compared to nontreated rats. A distinct elevation in the HbA1C, QT interval and a decline in the activity of catalase were also observed. Vitamin E treated rats shown significant decline in apoptosis, lipid peroxidation, protein carbonyl and QT interval compared to nontreated rats. Conclusion: Vitamin E decreased the incidence of apoptosis in cardiomyocytes, lipid peroxidation and improve antioxidant enzyme in the diabetic hearts of rats. Further research to confirm the findings is recommended.
Dr E Zarrinkalam, H Choobdari, Ms Emami, M Rasouli, Dr K Ranjbar,
Volume 23, Issue 5 (12-2021)
Abstract

Introduction: Exercise training has been suggested as a potential non-pharmacological strategy to prevent cardiovascular injuries. However, the role of exercise is controversial in preventing the progression of injuries caused by diabetic cardiomyopathy or their repairing. Therefore, this study aimed to evaluate the effect of aerobic exercise training on left ventricular apoptotic and antioxidant indices in a high-fat diet and streptozotocin-induced type 2 diabetic rat model. Materials and Methods:  Twenty-four male Wistar rats, 7-8 weeks of age, were randomly divided into two groups of normal diet (n = 8, ND) and high-fat diet (n = 16, HFD). The high-fat diet rats were given a free diet containing 55% fat for four weeks. For diabetes induction, 30 mg/kg of streptozotocin (STZ) was injected intraperitoneally into obese rats. Diabetic rats were subdivided into two groups: control diabetic (n= 8, CD) and diabetic-training (n = 8, TD) groups. The training group performed aerobic exercises on a treadmill for four weeks. The normal diet and control diabetic groups did not receive any exercise training. Results: Diabetes caused left ventricular catalase activity (p=0.001) reduction and increased caspase-9 (p=0.001) and P53 (p=0.001). Exercise training increased the maximum oxygen consumption rate by 37% (p=0.003) in the diabetic rats. The TD group had lower HOMA-IR (p=0.01) and plasma glucose (p=0.003) than the CD group. Also, aerobic training increased catalase (p=0.01) but decreased caspase-9 (p=0.001) and P53 (p=0.005) in the diabetic rats. Conclusion: Progressive aerobic exercise training can contribute to insulin resistance amelioration by increasing catalase activity and reducing apoptotic indices. Therefore, aerobic exercise training can be used as an effective non-pharmacological method of treating diabetic cardiomyopathy.

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مجله ی غدد درون‌ریز و متابولیسم ایران، دو ماهنامه  پژوهشی مرکز تحقیقات غدد درون‌ریز و متابولیسم، Iranian Journal of Endocrinology and Metabolism
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