الفهرس 
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Abstract
Introduction : Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the world, with a prevalence of 20%. Hepatic steatosis is the first stage of NAFLD and is followed by liver injury in the next stage of the disease, called nonalcoholic steatohepatitis (NASH). The current study was designed to examine CXCR4 receptors expression and its cellular localization in liver in the control and NAFLD rat model. Animals and methods : A 24 adult male Sprague-Dawley rats were used in the experiment, with average weight ranging between ””200-250”” grams. The rats were randomly divided into control and experimental groups. group І (Control group): (6 rats) were received basal diet and ordinary drinking water. group ІІ (Experimental group), (High fat diet group): formed of 18 rats were received high fat diet plus fructose 20% in the drinking water. The rats were subdivided into 3 subgroups; group ІІa : (6 rats) were sacrificed after 6 week, group ІІb : (6 rats) were sacrificed after 8 weeks and group ІІc : (6 rats) were sacrificed after 12 weeks . Results : Administration of high fat diet and fructose succeeded to establish NAFLD model, and this was confirmed by biochemical, histopathological and immunohistochemical techniques. The high fat diet subgroups showed establishment of model of progressive NAFLD evidenced by progressive elevation of liver enzymes and elevation of total cholesterol and triglycerides levels and changing the liver structure from steatosis up to distortion of the whole liver in the 12th weeks group.Examination of oil red stained sections showed progressive increase in the amount of fat droplets which were marked after 12 weeks of administration of high fat diet and fructose and image analysis of the sections showed significant increase in the area of oil red stain in all of the high fat diet groups.Examination of Sirius red stained sections showed progressive fibrosis noticed in the 6th weeks HFD group evidenced by increased amount of Sirius red stained areas followed by appearance of fibrous tissue septa at 8th weeks HFD group then distortion of liver architecture with thick fibrous tissue septae and pseudo-lobules formation in 12th weeks HFD group with significant increase in Sirius red stained area. Immunohistochemical staining showed positive immune reactivity in the control group. In high fat diet groups there was increase in the optical density of cxcr4 receptors with different cellular localization. At the 6th weeks group was detected in hepatocytes only, then increased progressively and appeared in most of hepatocytes and some cells in the fibrous septa and by the 12th weeks group it was detected in most of hepatocytes and fibrous tissue septa. Conclusion: CXCR4 immunoreactivity in NAFLD model increases progressively with progression of the injury from simple steatosis to steatohepatitis and fibrosis.