NGF Induced Activated HSCs Apoptosis In Hepatic Fibrotic Rat Via P75 Receptor

It is well known that the main reseasion of liver fibrosis is that hepatic stellate cells(HSCs)become active. The increasing of production and secretion of extracellular matrix(ECM)and the decreasing of degradation of them result in the accumulation of over ECM in the liver. HSCs are the most important cells during the formation of liver fibrosis. The activation and proliferation of HSCs are the critical events in the pathogenesis of hepatic fibrosis. So the significant strategy of preventing liver fibrosis is to inhibit proliferation and induce apoptosis of HSCs.There are apoptosis and proliferation of cells in dissimilar degree in normal livers and all kinds of injuried livers. During the formation of liver fibrosis,the amount of HSCs are overall increasing. In the period of recovery,the apoptosis of HSCs increase significantly. Apoptosis and proliferation of cells are antithetic continuums to preserve relative stability of body. So they play a key role in the formation and resolution of hepatic fibrosis.The formation of liver fibrosis is a slow and complex process. The base of molecule pathology is that they secrete cytokines after liver tissues are stimulated by pathogenic factors. When cells,ECM and cytokines are interacting,the metabolisms of ECM are disarray and ECM accumulate in the Disse diastema. Then,hepatic sinusoid is formed.In recent years,Trim et al discovered that after HSCs were incubated in 100ng/mL NGF for 24hr,the amount of apoptosis of HSCs significantly increased. NGF induced apoptosis of HSCs in dose-dependent manner. But no effect of NGF on proliferation of HSCs. These data demonstrated that NGF could induce apoptosis of activated HSCs were cultured outside body. The mechanisms might refer to the interaction of NGF and p75. However,...