Objective: Hepatic Fibrosis is a necessary pathological procession, through which various chronic liver diseases develop to hepatic cirrhosis. Its formation and development is closely linked to the prognosis and turnover of many liver diseases. If the liver inflammation, which is the initiating agent of liver injury, is controlled efficiently, the liver injury can be slowed down, what follows next the hepatic fibrosis can be prevented well. When impaired factors persistently stimulate the liver, HSC is activated and its phenotype transforms into myofibroblast which can secrete massive ECM. That is the key course of occurrence and development in hepatic fibrosis. After HSC become active, its phenotype is very hard to be reversed, NGF can lessen the inflammation through inhibiting the activity of NF- B, in addition through its receptor of P75 NGF can mediate apoptosis, which can decrease the number of the active HSC and not initiate inflammation damage of microenvironment. So the role of NGF in hepatic fibrosis has gradually been admitted by people. The objective of this experiment is to research whether exosomatic NGF can prevent or reverse the hepatic fibrosis in the intact animal model of hepatic fibrosis.
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