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AIM:To investigate the role of nuclear factor-kB (NF-kB)inhibitor caffeic acid phenethyl ester (CAPE) in theproliferation,collagen synthesis and apoptosis of hepaticstellate cells (HSCs) of rats.METHODS:The HSCs from rats were isolated and culturedin Dulbecco’s Modified Eagle’s Medium (DMEM) and treatedwith CAPE.The proliferation and collagen synthesis of HSCswere determined by ~3H-TdR and ~3H-proline incorporationrespectively,and the expression of type Ⅰ,Ⅲ procollagengenes was further explored by in situ hybridization.Apoptosiscell indices (AIs) were examined using terminaldeoxynucleotidyl transferase- mediated DIG-dUTP nick endlabeling (TUNEL).RESULTS:In activated HSC in culture,CAPE significantlyinhibited ~3H-TdR and ~3H-proline incorporation by HSCs atconcentrations of 5 μmol/L and 10 μmol/L respectively.CAPEalso reduced the type I procollagen gene expression (P<0.05)at higher concentration.Apoptosis of HSC was induced byCAPE and the AIs were time-and dose-dependently increasedfrom 2.82±0.73 % to 7.66±1.25 % at 12 h (P<0.01) andfrom 3.15±0.88 % to 10.61±2.88 % at 24 h (P<0.01).CONCLUSION:CAPE inhibits proliferation and collagensynthesis of HSC at lower concentration and induces HSCapoptosis at higher concentration.
AIM: To investigate the role of nuclear factor-kB (NF-kB) inhibitor caffeic acid phenethyl ester (CAPE) in theproliferation, collagen synthesis and apoptosis of hepaticstellate cells (HSCs) of rats. METHODS: The HSCs from rats were isolated and culturedin Dulbecco’s Modified Eagle’s Medium (DMEM) and treated with CAPE. Proliferation and collagen synthesis of HSCs were determined by ~ 3H-TdR and ~ 3H-proline incorporation was observed, and the expression of type I, III procollagengenes was further explored by in situ hybridization. Apoptosis cell indices (AIs) were examined using terminal deoxynucleotidyl transferase-mediated DIG-dUTP nick end labeling (TUNEL) .RESULTS: In activated HSC in culture, CAPE significantly inhibited ~ 3H-TdR and ~ 3H-proline incorporation by HSCs at concentrations of 5 μmol / L and 10 μmol / L respectively.CAPEalso reduced the type I procollagen gene expression (P <0.05) at higher concentration. Apoptosis of HSC was induced by CAPE and the AIs were time-and dose-dependently increas edfrom 2.82 ± 0.73% to 7.66 ± 1.25% at 12 h (P <0.01) and from 3.15 ± 0.88% to 10.61 ± 2.88% at 24 h (P <0.01) .CONCLUSION: CAPE inhibits proliferation and collagensynthesis of HSC at lower concentration and induces HSCapoptosis at higher concentration.