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Pharmacological Study On The Protective Action Of Bicyclol Against Experimental Liver Injury And Fibrosis In Animals

Posted on:2002-02-05Degree:DoctorType:Dissertation
Country:ChinaCandidate:Y LiFull Text:PDF
GTID:1104360185968888Subject:Biochemical pharmacology
Abstract/Summary:PDF Full Text Request
Liver plays a key role in metabolism and detoxification of many endobiotic and xenobiotics. Certain chemical toxins can directly or indirectly induce liver damage through their toxic metabolites generated in liver. Alcoholic liver disease, chronic viral hepatitis and liver cirrhosis are the common liver diseases all over the world, which seriously affected the health of patients. Although many drugs have been used in the treatment of chronic liver disease, however, no satisfied drug is available at present. To develop a new effective anti-hepatitis drug is very necessary.The new anti-hepatitis drug, 4,4'-dimethoxy-2, 3, 2', 3'-dimethylenedioxy-6-hydroxymethyl-6'-carbonyl-biphenyl (Bicyclol), is a derivative of its precursor Dimethyl Diphenyl Bicarboxynate (DDB), a known anti-hepatitis drug used in China for many years. Previous study indicated that Bicyclol had hepatoprotective action against experimental liver injury caused by certain toxins. Its effect was related to the modulation on liver cytochrome P450 activity, inhibition of lipid peroxidation, protection of cell membrane and DNA damage. Bicyclol also showed inhibitory effect on virus replication on duck viral hepatitis and 2.2.1.5 cells. Clinical trial showed that Bicyclol is effective on the treatment of chronic viral hepatitis B and C by decreasing of elevated ALT and AST, improving of symptoms and inhibiting of hepatitis B virus replication. In order to further investigate the hepatoprotective mechanism of Bicyclol, and provide basis for further clinical usage of Bicyclol, we studied the protective effect of Bicyclol on drug-, alcohol-induced liver injury and CCl4-induced liver fibrosis and its mechanism.
Keywords/Search Tags:Pharmacological
PDF Full Text Request
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