الفهرس 
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Abstract
Liver fibrosis is the wound healing response to a variety of acute and chronic stimuli, including, viral infection, ethanol, drugs, toxins, cholestasis, and metabolic disease. Hepatic fibrosis develops due to an increase in fibrillar collagen synthesis and deposition along with insufficient remodeling.
Apoptosis is one complications of fibrotic liver disease which leads to hepatic insufficiency which leads to hepatic death. Caspase- 3genes is an important marker of apoptosis, the increased activity of caspase -3 gene is mainly due to Apoptotic pathway is a direct activator of caspases as intracellular metabolic disturbances or excess reactive oxygen species can cause damage in mitochondria, which results in cytochrome C release and caspase-3 activation.
Hepcidin is produced primarily by hepatocytes. Other tissues and cells have been shown to express hepcidin, although to a much smaller extent. The hepcidin response to dietary iron is proportional to the increase in the amount of iron carried on plasma transferrin (i.e., transferrin saturation).
Hepcidin synthesis is regulated by a vast range of factors, including iron concentration, inflammation, and erythropoiesis. One key process, in particular, related the regulation of hepcidin, occurs through the bone morphogenic protein (BMP) pathway.
Hepcidin is the main regulator of iron metabolism and function by binding to the iron export protein ferroprotin which occur on the plasma membrane of reticuloendothelial cells mainly macrophages
The goal of this study is to know the effect of apoptosis on hepcidin gene expression and to measure the degree of correlation between hepcidin and caspase-3 genes and to prove that hepatic apoptosis and its regulation are thought of as a pivotal step in most forms of liver injury, including liver fibrosis, cirrhosis, and the development of hepatocellular carcinoma which needs further study that help in control of liver apoptosis and fibrosis.
In our study rats were divided into two groups normal group and group subjected to carbon tetrachloride (CCL4), rats subjected to carbon tetrachloride show fibrosis, The fibrosed liver tissue was analyzed for caspase -3 gene expression and hepcidin gene expression using Real Time RT- PCR also we measured iron level in serum and levels of serum liver enzymes, according to these results we found severity of apoptosis and classified our results into four groups.
We also found the negative correlation between caspase-3 and hepcidin gene expression. Also histopathological changes (apoptosis score) were measured in liver tissue, immunohistochemistry by immunohistochemical stain of caspase-3.
We conclude that that there is negative correlation between hepcidine and caspase 3 gene expressions. This may indicate that hepcidin gene expression may has a role in apoptosis or the apoptosis may affect the expression of this gene which needs further study that help in control of liver apoptosis and fibrosis.