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العنوان
The Beneficial Effects of Berberine on Experimental Model of Acrylamide Induced Nephrotoxicity /
المؤلف
El Gendy, Dalia Ahmed Mohamed.
هيئة الاعداد
باحث / Dalia Ahmed Mohamed El Gendy
مشرف / Nagah Kamel Gaafar
مشرف / Lamees Mohammed Dawood
مشرف / Nahla Anas Nasef
الموضوع
Biochemistry.
تاريخ النشر
2023.
عدد الصفحات
p 159. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
الأشعة والطب النووي والتصوير
تاريخ الإجازة
19/2/2023
مكان الإجازة
جامعة طنطا - كلية الطب - الاشعة التشخيصية
الفهرس
Only 14 pages are availabe for public view

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Abstract

Summary and conclusion Acrylamide (AA), a substrate for polyacrylamide synthesis, is widely used in many industrial fields, such as wastewater treatment, drinking water purification, and other industries including manufacturing paper, plastics and cosmetics. Also, large amounts of AA were detected in some carbohydrate rich-food produced at high temperatures. Therefore, people are inevitably exposed to AA in their daily life. Many animal studies have indicated that AA exhibits neurotoxicity, nephrotoxicity, genetic toxicity and reproductive toxicity. So AA has attracted widespread attention due to its harmful effects on human health. Nephrotoxicity can be defined as renal disease or dysfunction that arises as a direct or indirect result of exposure to medicines, industrial, and environmental chemicals. As the kidney excretes many drugs, it is routinely exposed to high concentrations of these drugs or their metabolites. AA induces nephrotoxicity via generation of free radicalsand the imbalance in the redox state which in turn leads to oxidative stress and inflammation. The NLRP3 inflammasome is one of the most studied inflammosomes and its activation enables inflammasome complex assembly, facilitating pro-caspase-1 cleavage to obtain active caspase1, followed by the release of mature IL-18 and IL-1β via pro-IL-18 and pro-IL-1β cleavage. NLRP3 inflammosome activation plays a central role in the pathogenesis of AA induced nephrotoxicity. Autophagy is the bulk degradation of cytosolic components, including aged or damaged proteins. Mitochondrial autophagy