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The Effects Of Long-term Alcohol Intake On Hepatocyte Apoptosis And Hepatic Fibrosis Liver Tissues Of Chronic Hepatitis B

Posted on:2008-09-08Degree:MasterType:Thesis
Country:ChinaCandidate:Y LiuFull Text:PDF
GTID:2144360218458982Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
OBJECTIVEThe purpose of this study was to investigate the relationships between alcohol intake with apoptosis and liver fibrosis of CHB patients. To elucidate the mechanism that alcohol intake could aggravate liver damage and liver fibrosis of CHB. And to provide a theoretical basis and new ideas to prevent from CHB liver fibrosis.METHODS52 cases liver biopsies of chronic hepatitis B virus patients from ChangHai hospital during 1998-01~1999-12 were selected. The patients were then categorized into chronic hepatitis B without alcohol intake group(CHB group) 27 patients,mean age 34.8±9.1 years; chronic hepatitis B alcohol group (CHB alcohol group)25 patients,mean age33.1±10.3 years; and 10 patients'normal liver tissues of resectable hepatic adjacent hemangioma, mean age33.5±9.3 years,used as a normal control group. Statistic data in three group patients on age, sex, duration of hepatitis B virus infection,serum alanine aminotransferase(ALT) and HBV DNA viral load. Liver tissues of the three groups were used to liver HE staining to observe and evaluate integral fibrosis; TUNEL detection of liver cell apoptosis; Immunohistochemical (Envision) of the expression of Fas antigen in liver were performed.RESULTSLiver fibrosis stage and hepatic apoptosis density of HBV alcohol group was significantly greater than HBV no alcohol group and control group. Expression of Fas (CD95) was found in HBV patients but not in controls.The degree of Fas expression correlated with Liver fibrosis stage or hepatocyte apoptosis as detected by terminal UTP nick end labelling (TUNEL). Frequent ethanol intake led to significant increase of hepatocyte apoptosis. Fas expression is correlated to fibrosis in HBV-infected patients and HBV with actively drinking ethanol.CONCLUSIONHBV leads to increased apoptosis of hepatocytes . Programmed cell death and and liver fibrosis can be further up-regulated by active ethanol consumption. The correlation between Fas expression and TUNEL supports the hypothesis that the Fas-Fas ligand interaction is the major mechanism for HBV-induced hepatocyte apoptosis and fibrosis. It indicates that long-term heavy drinking could aggragate liver apoptosis and fibrosis.The CHB patients must not drink;It may be profit clinical to prevent from liver injure and fibrosis to treat by anti-apoptosis.
Keywords/Search Tags:Ethanol, hepatitis B, liver tissue, hepatocyte, apoptosis, fibrosis, Fas
PDF Full Text Request
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