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العنوان
Study of the Protective Mechanisms of Thymoquinone in Experimentally Induced Myocardial Infarction in Rats/
المؤلف
Rashed, Marwa Medhet.
هيئة الاعداد
باحث / Marwa Medhet Rashed
مشرف / Ebtehal El-Demerdash Zaki
مشرف / Azza Sayed Awad
مشرف / Magdy Aly Hassan
تاريخ النشر
2015.
عدد الصفحات
252 p. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
الصيدلة ، علم السموم والصيدلانيات (المتنوعة)
تاريخ الإجازة
1/1/2015
مكان الإجازة
جامعة عين شمس - كلية الصيدلة - الأدوية والسموم
الفهرس
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Abstract

The present study was aimed to investigate the cardioprotective effect of TQ using two different doses in reducing isoprenaline-induced myocardial infarction and its effect with respect to lipid metabolism, oxidative stress, inflammation and apoptosis.
Male albino rats received TQ once daily for 7 consecutive days at doses of 10 and 20 mg/kg orally then two dose of ISP (85 mg/kg; S.C.) on 6th &7th day with 24 hour interval. Animals were sacrificed 24 hours after last injection of isoprenaline.
The present study showed that ISP caused significant myocardial damage in rats, which was characterized by increased heart rate, conduction abnormalities, heart index, serum CK-MB, apoptotic nuclei counts, 26% infarction size and myofibrillar disarrangement. Thymoquinone pre-treatment particularly at dose of 20mg/kg significantly protected against myocardial damage induced by ISP.
Furthermore, ISP induced lipid profile alteration expressed as elevation in Triglyceride, Cholesterol and LDL with reduction in HDL. These lipid alterations were modified by pre-treatment with TQ at dose 20mg/kg. As indicators of oxidative stress, ISP caused significant GSH and depletion, lipid peroxidation and reduction in total antioxidant activities.Pre-treatment with TQ significantly attenuated ISP-induced oxidative injury in cardiac tissue. Furthermore, ISP induced apoptotic tissue damage by increasing the expression of caspases 3&9 activities and cytochrome c content. TQ pre-treatment ameliorated these apoptotic actions of ISP. Moreover, ISP induced increased the expression of TNF-α and NF-κB which further promote the ISP-induced apoptotic cell death. On the contrary, TQ pre-treatment effectively neutralised all these effects. Collectively, these findings indicate that TQ possesses a potent protective effect against ISP-induced cardiotoxicity via inducing hypolipidemic effect and suppressing oxidative stress and apoptotic tissue damage.
In conclusion TQ especially at dose 20mg/kg possesses a potent protective effect against ISP-induced cardiotoxicity via inducing hypolipidemic effect, anti-inflammatory effect and suppressing oxidative stress and apoptotic tissue damage.