الفهرس 
Pathogenesis of NAFLDOnly 14 pages are availabe for public view
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Abstract
Background:
Fenofibrate( FF) is a hypolipedmic drug and one of PPARα agonists which is a drug target for Non alcoholic Fatty liver disease (NAFLD), it increases homocystiene (Hcy) which was linked to a variety of inflammatory and oxidative disorders.
Aim: the present study was done to compare the effect of FF (when administrated alone or with Folic acid (FA)) of Gemfibrozil (GF) on the prognosis of NAFLD in male albino rats.
Methods: Eight groups (6 rats each) of male Wister rats were divided into 2 main groups, group I subdivided into control and High Fat diet (HFD) groups, which subdivided to HFD-untreated, HFD-FF, HFD-FF-FA and HFD-GF-treated groups. group II subdivided into control naïve, FF-treated and GF-treated groups.
The doses used for FF and GF were 100 mg/Kg/day and FA 10mg/kg/day received by oral gavage in the last 6 weeks of the experiment which lasts for 14 weeks in group I and 6 weeks in group II.
Body weight (BW), Glomerular Filtration Rate (GFR), biochemical markers (serum creatinine (S.cr), plasma Hcy, lipid profile, liver enzymes and liver fibrosis markers), liver index, renal perfusion (RP) and histopathological studies were performed.
Results: HFD- untreated group as a model of NAFLD produced significant increase (P<0.05) in BW, S.cr, plasma Hcy, total cholesterol, Triglycerides (TG), low-density lipoprotein (LDL), liver enzymes and liver fibrosis markers, liver index and scores in histopathological results with significant decrease in high-density lipoprotein (HDL), GFR and RPT when compared to control group.
HFD-FF treated group produced significant decrease (P<0.05) in BW, total cholesterol, TG, LDL, liver enzymes and liver fibrosis markers with significant increase (P<0.05) in HDL and Liver index when compared to HFD untreated group.
Adding FA to FF in HFD-FF-FA treated group produced significant decrease (P<0.05) in S.cr. plasma Hcy, total cholesterol, TG, LDL, liver enzymes and liver fibrosis markers when compared to HFD-FF- treated group. Also, HFD-GF-treated group associated with significant decrease (P<0.05) in S.cr, plasma Hcy, total cholesterol, TG, LDL, liver enzymes, liver fibrosis markers and score of steatosis in histopathological results and produced significant increase (P<0.05) in HDL, GFR and RP when compared to HFD-FF- treated group.
Conclusion: This work clarifies the preference of adding FA to FF over FF alone and the preference of GF over both FF and FF-FA in model of NAFLD in rats.