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العنوان
Possible Anti-Oxidant Effect of Calcium Channel Blockers in Suppression of Atherosclerosis in Cholesterol-Fed Rabbits /
الناشر
Mohamed Abd Ellah Ibraheem,
المؤلف
Ibraheem, Mohamed Abd Ellah.
هيئة الاعداد
باحث / Mohamed Abd Ellah Ibraheem
مشرف / Mohamed Montaser A. Khalifa
مشرف / Magdy Kassem A. Hassan
الموضوع
Pharmacology Calcium Anti-Oxidant Atherosclerosis Fed Rabbits Cholesterol Calcium Channel Blockers
تاريخ النشر
1998 .
عدد الصفحات
176 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
علم الأدوية (الطبية)
تاريخ الإجازة
1/1/1998
مكان الإجازة
جامعة المنيا - كلية الطب - Pharmacology
الفهرس
Only 14 pages are availabe for public view

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from 202

Abstract

In the present study an attempt was undertaken to investigate any possible antiatherogenic properties of some calcium channel blockers against atherosclerosis induced by 1% cholestrol feeding.
The drugs selected for this investigation include diltiazem and nicardipine.
In the present study, male new zealand white rabbits were subjected to an atherogenic diet and were classified into for main groups; normal control control atherosclerotic,
- treated atherosclerotic; and nicardepine-treated atherosclerotic groups.
Diltiazem was administrated intraperitoneally and nicardipin was administrated intramuscularly for 2 months.
The results obtained in the present study clearly demonestrated that:
Oral administration of cholesterol 1% produced significant increase of the body weight of the rabbits in each group after 4 and 8 weeks. Also oral administration of diltiazem and nicardipin produced non-significant change in the body weight.
from the present work , it can be deduced that atherosclerosis in rabbits is accompanied by an increase oxygen free radicals formation that account for the increased lipid peroxidation, as well as a marked decrease of the antioxidant defense mechanism represented by the decrease in the activity of the anti oxidant enzymes. This can contribute to the pathogenesis of atherosclerosis.
We conclude that nicardepine and dilitazem have protective effects from lipid peroxidation, which may be mediated via tissue glutathione peroxidase enzyme.