Possible modulation of inflammator mediatiors and hepatic fibrosis by an angiotensin II receptor blocker (ARB) in a rat model of CC14-induced liver injury /
Sara Abdelmgeed Hamed Elwakeel
Possible modulation of inflammator mediatiors and hepatic fibrosis by an angiotensin II receptor blocker (ARB) in a rat model of CC14-induced liver injury / التغيرات التى يمكن حدوثها للوسطاء الالتهابية والتليف الكبدى باستخدام مثبطات مستقبلات الانجيوتنسين 2 فى نموذج للجرذان المصابة بتليف كبدى ناجم عن استخدام رابع كلوريد الكربون Sara Abdelmgeed Hamed Elwakeel ; Supervised Ezz Eldin S. Eldenshary , Moushira Ibrahim Elsayed , Noha N. Nassar - Cairo : Sara Abdelmgeed Hamed Elwakeel , 2013 - 90 P. : charts , facsimiles ; 25cm
Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology
Hepatic fibrosis is defined as a wound healing response to liver injury characterized by the deposition of extracellular matrix (ECM). The duration of insult is a crucial parameter managing the extent of injury. Whereas an acute insult provokes transient changes and the normal hepatic architecture is regenerated, a more persistent injury results in sustained chronic inflammation and accumulation of ECM leading to progressive substitution of liver parenchyma by scar tissue
Angiotensin II Hepatic fibrosis Liver injury
Possible modulation of inflammator mediatiors and hepatic fibrosis by an angiotensin II receptor blocker (ARB) in a rat model of CC14-induced liver injury / التغيرات التى يمكن حدوثها للوسطاء الالتهابية والتليف الكبدى باستخدام مثبطات مستقبلات الانجيوتنسين 2 فى نموذج للجرذان المصابة بتليف كبدى ناجم عن استخدام رابع كلوريد الكربون Sara Abdelmgeed Hamed Elwakeel ; Supervised Ezz Eldin S. Eldenshary , Moushira Ibrahim Elsayed , Noha N. Nassar - Cairo : Sara Abdelmgeed Hamed Elwakeel , 2013 - 90 P. : charts , facsimiles ; 25cm
Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology
Hepatic fibrosis is defined as a wound healing response to liver injury characterized by the deposition of extracellular matrix (ECM). The duration of insult is a crucial parameter managing the extent of injury. Whereas an acute insult provokes transient changes and the normal hepatic architecture is regenerated, a more persistent injury results in sustained chronic inflammation and accumulation of ECM leading to progressive substitution of liver parenchyma by scar tissue
Angiotensin II Hepatic fibrosis Liver injury