Search In this Thesis
   Search In this Thesis  
العنوان
Possible Protective Effect of Telmisartan in Experimentally-Induced Peptic Ulcer in Rats
الناشر
Remon Roshdy Rofaeil Gerges,
المؤلف
Gerges, Remon Roshdy Rofaeil
هيئة الاعداد
باحث / Remon Roshdy Rofaeil Gerges
مشرف / Osama M. Ashour
مشرف / Mohamed Aly M. Morsy
مشرف / Entesar F. Amin
الموضوع
Telmisartan Pharmacology Peptic Ulcer in Rats Pharmacology
تاريخ النشر
2008 .
عدد الصفحات
177p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب (متفرقات)
تاريخ الإجازة
21/1/2008
مكان الإجازة
جامعة المنيا - كلية الطب - Pharmacology
الفهرس
Only 14 pages are availabe for public view

from 191

from 191

Abstract

The present investigation aimed to evaluate the gastroprotective effect of telmisartan in indomethacin- and CRS-induced ulcer models in rats. In addition, the possible mechanism(s) of such protection were also investigated by measuring acidity, pepsin, mucin, lipid peroxides, PGE2 and NO. Results of the present study clearly demonstrated that:
• Ulcerative lesions were observed in indomethacin-treated and CRS rats; the ulcer indices mounted to 72.7 ± 11.6 and 59.7 ± 11.8, respectively. In both models, there was a significant reduction in pH, increase in F.A.C., T.A.C., F.A.O., T.A.O. and both pepsin concentration and output and also a significant reduction in mucin concentration. At the same time, significant increase in MDA, reduction in NO and PGE2, were noticed.
• Pretreatment of indomethacin-treated and CRS rats with ranitidine significantly protected rats from gastric mucosal ulceration and reduced the ulcer indices to 7.67 ± 1.58 and 7.47 ± 2.78, respectively, achieving preventive indices 89.4 and 87.5%, respectively. Pretreatment of indomethacin subgroup with ranitidine caused significant reduction in gastric juice volume, while, in both models, ranitidine significantly increased pH and significantly decreased F.A.C., T.A.C., F.A.O., T.A.O., pepsin output and significantly increased mucin concentration. At the same time, ranitidine significantly reduced gastric mucosal MDA, increased NO and PGE2, as compared to the ulcer non-treated subgroups.
• Pretreatment of indomethacin and CRS-treated rats with candesartan significantly reduced gastric lesions ulcer indices to, 31.1 ± 2.7 and 28.1 ± 1.82, respectively, achieving preventive indices of 57.2 and 52.9%, respectively. Only in indomethacin-treated rats, candesartan reduced F.A.O., T.A.O. and pepsin output. In both models, candesartan significantly decreased MDA and PGE2, as compared to the ulcer non-treated subgroups.
• Pretreatment of indomethacin-treated rats with telmisartan, in doses of 1, 3 and 10 mg/kg, significantly protected rats from gastric ulceration and reduced the ulcer indices to 20.7 ± 1.27, 14.8 ± 2.85 and 10.2 ± 1.51, respectively, achieving preventive indices of 71.6, 79.6 and 85.9%, respectively. On the other hand, Pretreatment of CRS rats with telmisartan, in doses of 1, 3 and 10 mg/kg, significantly protected rats from gastric ulceration and reduced the ulcer indices to 24.5 ± 3.27, 19.1 ±4.28 and 11.7 ± 3.87, respectively, achieving preventive indices of 59, 68 and 80.4%, respectively. In both models, The highest dose produced comparable results to ranitidine-treated rats. Pretreatment of indomethacin-treated rats with telmisartan significantly reduced F.A.O., T.A.O. and pepsin output. In both models, Telmisartan (3 and 10 mg/kg) significantly reduced MDA and significantly increased total nitrites as compared to the ulcer non-treated subgroup; while, PGE2 was not altered by telmisartan, in the three dose levels.