الاثنين، 24 أغسطس 2015

أطروحة الماجستير للطالبة رويدا محمد بنيان

 ناقشت بنجاح طالبة الماجستير رويدا بنيان من قسم الصيدلة السريرية يوم الأحد 16/8/2015م بعنوان:
Evaluation of the role of spironolactone on myocardial oxidative stress in rat model of streptozotocin-induced diabetes
وقد ضمت لجنة المناقشة الدكتورة فاديا مياس رئيسا وعضوية كل من الدكتور كارم الزعبي والدكتور محمد خطاطبه والدكتور عمر قموه كممتحن خارجي.

باسم صفحة أصدقاء كلية الصيدلة_ في جامعة العلوم والتكنولوجيا الأردنية نبارك للطالبة رويدا بنيان إتمامها درجة الماجستير في الصيدلة السريرية بنجاح متمنين لها مزيدا من التقدم والنجاح.

* للاطلاع على ملخص الدراسة:

Background: Diabetes mellitus is a common chronic disease that has been linked to the development and progression of heart failure and other cardiovascular diseases (CVDs). Several mechanisms may contribute to the substrates of CVDs during diabetes such as inflammation, impaired hormonal regulation and oxidative stress. Recently, oxidative stress has gained attention as a key player. Oxidative stress is determined by the imbalance between the generation of reactive oxygen species (ROSs) and the antioxidant defenses in the body. ROSs generation promotes cellular dysfunction and damage by sequence of inflammatory, structural and apoptotic processes. The rennin angiotensin aldosterone system (RAAS) is involved in the pathophysiology of CVDs. Aldosterone is an adrenal hormone, and a critical modulator of blood pressure and electrolytes balance. Aldosterone contributes to cardiac inflammation, oxidative stress, and remodeling. The angiotensin converting enzyme inhibitors or receptor antagonists are key cardio and reno-protective medications for patients with DM and underlying CVDs. Spironolactone, an aldosterone antagonist, has been also shown to improve cardiac function and to attenuate cardiac remodeling. The impact of aldosterone antagonist on myocardial oxidative status in DM is unclear

Aim: To evaluate short term impact of streptozotocin induced DM (single injection 35mg/Kg) on myocardial aldosterone levels, ROSs, and oxidative stress markers, and to determine the effects of four weeks treatment with spironolactone on myocardial ROSs levels, and oxidants/antioxidants markers in diabetic rat model

Method: Young adult Sprague Dawley rats weighing (245-340 g) were randomly assigned into four groups (12-15 each); normal rats (control), normal rats treated with 50 mg/kg spironolactone (Spir), diabetic rats (DM), and diabetic rats treated with 50 mg/kg spironolactone (DM+Spir) for 4 weeks. Body weight and blood glucose were measured at baseline and throughout the study. Blood pressure was measured at base line and at the end of the study. At the terminal day, blood samples were collected to measure serum lipids, glycated hemoglobin (HbA1c) and glucose levels. Cardiac tissues were homogenized for measurements of aldosterone levels and oxidants/ antioxidants markers

Result: The use of STZ induced DM and increased the percentage of HbA1c, but did not cause dyslipidemia, hypertension or cardiac dilation in both spironolactone treated and untreated rats. Relative to control, a significant increase in aldosterone levels was observed in the DM and DM+Spir groups. This increase was paralleled with a significant increase in total nitrite levels (ROSs form) and a significant reduction in vitamin E antioxidant levels in the DM group. Use of spironolactone reduced total nitrite levels and improved vitamin E cardiac levels. A significant increase in glutathione reductase / peroxidase activities was observed in the DM and DM+Spir groups without changes in the ratio of reduced to oxidized form of glutathione (GSH/GSSG). Relative to control, a significant increase in superoxide dismutase (SOD) and catalase activities was observed in the DM group. Cardiac lipid peroxidation products (TBARS) were similar among the groups

Conclusions: Our study suggests that STZ induced-DM is associated with increased myocardial aldosterone levels and total nitrite (ROSs form) formation. Use of spironolactone reduced nitrite generation and improved vitamin E antioxidant levels independent of blood pressure lowering effect. The increase in total nitrite in DM promoted significant compensatory increases in enzyme antioxidant activities of SOD, catalase and GSH peroxidase/reducatase probably to reduce excessive ROSs generation and to prevent cardiac oxidative damage as observed by the lack of cardiac changes in TBARS and GSH/GSSG levels




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