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العنوان
The Impact Of Quercetin On Sirtuin 1, High Mobility group Box 1 And selected Oxidative Stress Indices In Ulcerative Colitis Induced By Oxazolone In Rats /
المؤلف
Oqela, Aya Fathi Mohmed.
هيئة الاعداد
باحث / ايه فتحى محمد عقيله
مشرف / يحي احمد المشد
مشرف / سامية عبد الحميد الدرديرى
مشرف / هبة بسيونى غانم
الموضوع
Biochemistry. Biochemistry. Medical Biochemistry.
تاريخ النشر
2019.
عدد الصفحات
147 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الكيمياء الحيوية (الطبية)
تاريخ الإجازة
20/2/2019
مكان الإجازة
جامعة طنطا - كلية الطب - Medical Biochemistry
الفهرس
Only 14 pages are availabe for public view

from 199

from 199

Abstract

Summary Ulcerative colitis is a chronic idiopathic inflammatory disease of the gastrointestinal tract that affects the large bowel and is a major disorder under the broad group of conditions termed inflammatory bowel disease. It is characterized by colonic mucosal ulceration, manifested mainly with abdominal pain, rectal bleeding, fecal urgency and diarrhea. Long standing cases may develop CRC which is one of the great challenges facing those patients.
The precise etiology of UC is still unknown, but it is thought to be multifactorial, involving genetic, immunologic, and environmental factors. So that ulcerative colitis result from aberrant immune response to specific components of the intestinal microbiota in genetically susceptible hosts, with clinical flares of the diseases initiated and reactivated by environmental factors.
HMGB1 is an important mediator of IBD as well as a new target for therapy. Also it is associated with many severe inflammatory and autoimmune diseases, such as sepsis, acute pancreatitis, acute lung injury, rheumatoid arthritis, and systemic lupus erythematosus. It is a highly conserved, non-histone nuclear protein that functions to stabilize nucleic acid structure and modulate gene transcription and expression. Moreover, HMGB1 can be released into the cytoplasm and even the extracellular milieu from activated inflammatory cells or necrotic cells, which then triggers inflammation. Hyperacetylation of HMGB1 affects its DNA binding and redirects it toward the cytoplasm. Also HMGB1 expression