Role of nitric oxide in experimentally induced liver fibrosis / Yasmin Shokr Mohamed ; Supervised Azza M. Agha , Hesham A. Salem , Lamiaa A. Ahmed

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Yasmin Shokr Mohamed

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Material type: Text

TextLanguage: English Publication details: Cairo : Yasmin Shokr Mohamed , 2015Description: 143 P. : charts , facsimiles ; 25cmOther title:

درا{uئإآ٣}{uئإ٩٤} دور أكسيد ا{uئإؤئ}{uئإإ٨}{uئإئ٤}{uئإ٩٨}{uئإءإ}{uئإئ٣}{uئإؤء} {uئإؤ٣}{uئإئ٢} {uئإ٩٧}{uئإإ٠}{uئإئ٤}{uئإؤ٢} ا{uئإؤئ}{uئإؤأ}{uئإ٩٢}{uئإءء} ا{uئإؤئ}{uئإإ٤}{uئإء٤}{uئإءء}ث {uئإ٩٧}{uئإء٠}{uئإءإ}{uئإئ٣}{uئإ٩٢}{uئإئ٤}{uئإ٨إ} [Added title page title]

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Dissertation note: Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology Summary: The present study was directed to investigate the possible hepatoprotective effect of nicorandil and to investigate the role of NO donation and KATP channel opening in its possible mediated protection in BDL-induced liver fibrosis in rats. Cholestasis is considered one of the most common causes of liver fibrosis with minimum therapeutic choices. It causes many pathological alterations in liver tissues, which include oxidative stress, inflammation, bile duct proliferation and HSCs activation. HSCs activation leads to proliferation, contractility, fibrogenesis, chemotaxis, matrix deposition and cytokines release. The current investigation included preliminary experiments in order to choose the suitable duration for induction of fibrosis by BDL without nodules formation in addition to the proper hepatoprotective dose of nicorandil and the best time for nicorandil administration. In the present study, BDL was used as a model for cholestasis. Liver fibrosis was induced after 14 days of BDL. The hepatoprotective effect of nicorandil (3mg/kg/day) was investigated in BDL in rats. In order to determine the mechanism by which nicorandil produced its hepatoprotective effect, glibenclamide (10mg/kg/day) or L-NAME (15mg/kg/day) were co-administration with nicorandil in another 2 groups

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Holdings
Item type	Current library	Home library	Call number	Copy number	Status	Date due	Barcode
Thesis	قاعة الرسائل الجامعية - الدور الاول	المكتبة المركزبة الجديدة - جامعة القاهرة	Cai01.08.09.M.Sc.2015.Ya.R (Browse shelf(Opens below))		Not for loan		01010110068019000
CD - Rom	مخـــزن الرســائل الجـــامعية - البدروم	المكتبة المركزبة الجديدة - جامعة القاهرة	Cai01.08.09.M.Sc.2015.Ya.R (Browse shelf(Opens below))	68019.CD	Not for loan		01020110068019000

Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology

The present study was directed to investigate the possible hepatoprotective effect of nicorandil and to investigate the role of NO donation and KATP channel opening in its possible mediated protection in BDL-induced liver fibrosis in rats. Cholestasis is considered one of the most common causes of liver fibrosis with minimum therapeutic choices. It causes many pathological alterations in liver tissues, which include oxidative stress, inflammation, bile duct proliferation and HSCs activation. HSCs activation leads to proliferation, contractility, fibrogenesis, chemotaxis, matrix deposition and cytokines release. The current investigation included preliminary experiments in order to choose the suitable duration for induction of fibrosis by BDL without nodules formation in addition to the proper hepatoprotective dose of nicorandil and the best time for nicorandil administration. In the present study, BDL was used as a model for cholestasis. Liver fibrosis was induced after 14 days of BDL. The hepatoprotective effect of nicorandil (3mg/kg/day) was investigated in BDL in rats. In order to determine the mechanism by which nicorandil produced its hepatoprotective effect, glibenclamide (10mg/kg/day) or L-NAME (15mg/kg/day) were co-administration with nicorandil in another 2 groups

Issued also as CD

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