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Study On The Mechanism Of Qizhu Recipe And Its Effective Monomer Astragalus Monomer Against Hepatitis B Hepatic Fibrosis Iron Metabolism Disorder

Posted on:2019-11-11Degree:MasterType:Thesis
Country:ChinaCandidate:Z H YeFull Text:PDF
GTID:2434330566468965Subject:Pharmacy
Abstract/Summary:PDF Full Text Request
Hepatitis B is a highly endemic area in China,and the number of patients who die of hepatitis B related diseases such as liver cirrhosis and hepatocellular carcinoma is increasing every year.Liver fibrosis is the necessary stage for the development of chronic hepatitis B to liver cirrhosis.How to prevent and cure hepatitis B has become an important problem in modern medicine.Most patients with chronic hepatitis B have liver iron metabolism disorder,excessive iron deposition in the liver,aggravating the damage of liver function,thus speeding up the process of liver fibrosis to liver cirrhosis,liver cancer transformation.If we can restrain this process effectively,it will delay the progress of the patient's condition,and thus improve the patient's quality of life and prolong the patient's life.Qizhu Fang is a clinical prescription,which has a good curative effect on chronic hepatitis B.However,the mechanism of Qizhu Fang in treating chronic hepatitis B is not clear.It has been reported that one of the mechanisms of Qizhu Fang on liver fibrosis in chronic liver diseases may be that it can reduce the activation factors of hepatic fibrosis and inhibit the synthesis of collagen by reducing the damage of liver cells,protecting the liver cells and alleviating the inflammatory reaction.In this paper,astragaloside A,an important component of astragalus membranaceus,was selected to study Qizhu Fang and astragaloside,respectively.The liver iron overload mouse model and cell model were established by using iron dextran as inducer.To study the protective effect of Qizhu Fang and astragaloside A on hepatic cell injury induced by iron overload.In the mouse model,compared with the positive control group,the total iron binding force increased,serum transferrin and alt AST decreased,and Qizhu Fang inhibited the increase of iron content in the liver and alleviated the iron accumulation in the liver caused by iron overload.Liver injury induced by iron overload may be closely related to lipid peroxidation and protein nitration.Qizhu Fang has goodantioxidation and anti-nitrification effects,thus effectively reversing liver injury caused by iron overload.In vitro cell experiment,after giving Qi Zhu Fang,the level of GSH increased significantly with the increase of Qizhu Fang.The levels of ALT,AST and MDA decreased significantly with the increase of the quantity of Qizhu Fang.It indicates that Qi Zhu Fang can effectively inhibit lipid peroxidation caused by iron overload.The level of T-BIL decreased significantly with the increase of the Qizhu Fang,the results showed that excessive iron content would cause hepatocyte damage,while Qizhu Fang could improve the hepatocyte damage induced by iron overload.Finally,astragaloside IV was used to treat liver injury induced by iron overload in mice.The contents of AST and ALT in serum of iron overload model group were significantly higher than those of blank control group.Serum iron level was significantly lower than iron overload model group,while TIBC increased significantly.MDA increased,and GSH decreased significantly.It shows that iron overload liver tissue has serious lipid peroxidation injury.The concentration of MDA in liver of different doses of astragaloside group decreased to varying degrees,however,the activity of GSH increased significantly,and the lipid peroxidation damage of liver was preliminarily deduced.It shows that different concentrations of astragaloside have a certain dose trend for alleviating the lipid peroxidation damage caused by iron overload.It is presumed that the mechanism of hepatic protective effect of astragaloside is probably related to its antioxidation.
Keywords/Search Tags:Qizhu Fang, Chronic hepatitis B, Hepatic fibrosis, Iron metabolic disorder, Astragaloside iv
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