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Abstract
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