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العنوان
The study of potential effect of some natural compounds on cardiotoxicity induced in experimental animals /
المؤلف
Al-Metwally, Salwa Reda Mohamed Abo El-Ela.
هيئة الاعداد
باحث / سلوى رضا محمد أبوالعلا المتولي
مشرف / ليلى أحمد عيسى
مشرف / راندا أحمد زغلول
مناقش / ممدوح محمد الششتاوي
مناقش / عاطف إبراهيم عبدالباقي
الموضوع
Cardiotoxicity. Cardiotoxicity - Experimental animals. Pharmacy. Biochemistry.
تاريخ النشر
2022.
عدد الصفحات
online resource (169 pages) :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الصيدلة ، علم السموم والصيدلانيات
تاريخ الإجازة
1/1/2022
مكان الإجازة
جامعة المنصورة - كلية الصيدلة - الكيمياء الحيوية
الفهرس
Only 14 pages are availabe for public view

from 169

from 169

Abstract

Doxorubicin (Dox) is an important chemotherapeutic agent, but unfortunately, is associated with serious cardiotoxicity. Baicalin (BAI) and catechin (CAT) are effective natural compounds. BAI and CAT are well-known for their anti-inflammatory and antioxidant effects. This study aimed to investigate the protective effects of BAI, CAT and their combination in attenuating Dox-induced cardiotoxicity. Methods : male Swiss albino mice were divided into five groups; control, Dox (2.5 mg/kg/every other day, i.p., 6 doses for 2 weeks), BAI (100 mg/kg/day, orally), CAT (100 mg/kg/day, orally), and BAI+CAT. Both BAI and CAT were administered two weeks previous to Dox and continued during Dox treatment. Key findings : Pretreatment with BAI and/or CAT significantly prevented Dox-induced elevation of serum activities of cardiac biomarkers and alterations to the heart. Moreover, BAI and/or CAT suppressed the gene overexpression of cardiac TLR4 and subsequently, prevented Dox-induced elevation of both cardiac NF-κB and IL-1β. BAI and/or CAT, also, significantly reduced the cardiac levels of DKK1 and elevated the level of β-catenin. Dox-induced elevation of MDA and reduction of GSH were reversed by BAI and/or CAT. Significance: BAI and CAT exhibited a significant cardioprotective effect against Dox-induced cardiotoxicity through the inhibition of the inflammatory TLR4/NF-κB pathway and the activation of the protective Wnt/β-catenin pathway by the suppression of DKK1.