Experimental Study Of The Mechanism To Preventing Hepatic Fibrosis And Compatibility By Gexiazhuyutang

Hepatic fibrosis (HF)is a common pathological histologic change during the process of cirrhosis, an ultimate result of variety kinds of liver diseases. The reason is ,the hepatic Stellate Cells are activated through regulation to cytokine and its network, hence to increase the synthesis of agents in extracellular matrix (ECM)while the degradation is relatively not enough that leads to the loss of dynamic equilibrium, and HF is therefore developed due to over-Sedimentation of ECM. In Western Countries, alcoholic is the most important reason that leads to HF but in our country, it is the hepatitis virus especially the continuous infection of type Band C of the virus that cause the disease, it is popularly believed at present that HF is reversible while cirrhosis is irreversible.The research includes two aspects: the theoretical research and the experimental research. The object of theoretical research is focusing on the understanding that In order to approach the mechanisms involved in the treatment to hepatic flbrosis (HF) with GXZYT, its effects on ALT.AST. pathologic histology and TIMP-1/2 in HF rats are observed. Furthermore, it has good effects on improvement of climic symptoms. From the ALA-Kokkol, the rat model of hepatic flbrosis is induced by abdominal injection of DMN, treating groups consist of GEXIAZHUYUTANG I , II , III .groups administrated with Colchicine Tablets is selected as control groups, and the treating started right after the model is established. The liver function (ALT\AST)is detected by biochemical method, levels of Serum procollagen III (pc-III )and hyaluronic acid (HA).LN are measured by radioimmunoassay. Iver Sections are made from the paraffin-embedded tissues and stained with hematoxylin and eosin and Mallory staining ,histological changes are observed under light microscope. The resuts of theresearch can be Summaried as follows: Theserum levels of ALT. AST. HA. LN and pc- III in model group is significantly higher, GEXIAZHUYUTANG can significantly lower the activity of ALT and AST of serum of liver tissue, The Serum levels of HA. LN. PC-III in treatment group and treatment control group significantly decreased compared to those in model group. The structure of hepatic lobules in model group is abnormal, there is no decrease in collagen fiber deposition, and sublobules is still remain. But infiltration of inflammatory cells decreased. In treatment and treatment control group, the structure of hepatic lobules in some degree recovered. Liver fatty metamorphosis and collagen fiber deposition degree scores are all decreased. There is no significant difference between treatment and treatment control group in the meantime, GEXIAZHUYUTANG can also decreased the expressions of TIMP-1/2 of model group. Conclusions: The result above expound the mechanism of anti-hepatoflbrosis of GEXZAZHUY -UTANG:(1)It can protect liver cell, lessen its degeneration and necrosis. Restore its structure and function, and improve the capillavilization of hepatic sinusoid and liver blood circulation.(2)It can downvegulate the expression of HA, LN that reveals both of HA and LN are closely related to hepatic fibrosis in LC.(3)It can inhibit the activation and proliferation of HSC, reduce the deposition of collagen of type III,inhibit or reverse the liver flbrosis.(4)It can also decrease the activity of TIMP-1/2 of liver flbrosis, improve the over-sedimentation of ECM.