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Effects Of Neutral Lipids And Tumor Necrosis Factor α On Biological Behavior Of Normal Adult Hepatocyte

Posted on:2005-01-04Degree:MasterType:Thesis
Country:ChinaCandidate:L SongFull Text:PDF
GTID:2144360155973251Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective: To explore the effects of very low density lipoprotein(VLDL), oxidized very low density lipoprotein(OX-VLDL) and tumor necrosis factor α (TNF-α) on proliferation of normal human hepatocyte and synthesis of hyaluronic acid(HA). To explore if VLDL, OX-VLDL and TNF-α can induce apoptosis.Methods: Normal adult hepatocytes were cultivated with VLDL, OX-VLDL and TNF-α of 3 different concentration respectively in serum-free culture medium for 48 hours. Effects of VLDL, OX-VLDL and TNF-α on proliferation of normal adult hepatocyte line and synthesis of hyaluronic acid were observed by means of MTT measuring and radioimmunoassay, respectively. The effects of TNF-α and VLDL or TNF-α and OX-VLDL were also observed. Flow cytometry were used to assess apoptosis rate.Results:1 Cell proliferation of every treated group was decreased. With doses increased, there was a decreased trend of cell proliferation. The VLDL-treated group of 80μg/ml, OX-VLDL -treated group of 40μg/ml and 80μg/ml and TNF-α-treated group of 1000u/ml and 2000u/ml weresignificant lower than control group(P<0.05).2 HA of all treated groups, except VLDL-treated group of 20ug/ml, TNF-a-treated group of 500u/ml and OX-VLDL -treated group of 80ug/ml,was significant higher than control. HA of OX-VLDL -treated group of 80ug/ml was significant lower than control.3 OX-VLDL, in corporation with TNF-a can induce apoptosis. Conclusion: 1 Excess of lipids and TNF-a in the liver might damagehepatocyte, and the effects of two factors together on hepatocyte were stronger than one factor alone. 2 Excess of lipids and TNF-a in the liver might induce fibrosis by promoting the synthesis of extracellular matrix .
Keywords/Search Tags:hepatocyte, culture, lipoprotein, hyaluronic acid, apoptosis
PDF Full Text Request
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