摘要
AIM: To investigate the role of nuclear factor-κB (NF-κB)inhibitor caffeic acid phenethy1 ester (CAPE) in the proliferation, collagen synthesis and apoptosis of hepatic stellate cells (HSCs) of rats.
METHODS: The HSCs from rats were isolated and cultured in Dulbecco's Modified Eagle's Medium (DMEM) and treated with CAPE. The proliferation and collagen synthesis of HSCs were determined by 3H-TdR and 3H-proline incorporation respectively, and the expression of type Ⅰ, Ⅲ procollagen genes was further explored byin situ hybridization. Apoptosis cell indices (AIs) were examined using terminal deoxynucleotidyl transferase- mediated DIG-dUTP nick end labeling (TUNEL).
RESULTS: Tn 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. CAPE also 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 increased from 2.82+0.73 % to 7.66±1.25 % at 12 h (P<0.01) and from 3.15±0.88 % to 10.6L±2.88 % at 24 h (P<0.01).
CONCLUSION: CAPE inhibits proliferation and collagen synthesis of HSC at lower concentration and induces HSC apoptosis at higher concentration.
AIM:To investigate the role of nuclear factor-kB (NF-kB) inhibitor caffeic acid phenethyl ester (CAPE) in the proliferation,collagen synthesis and apoptosis of hepatic stellate cells (HSCs) of rats. METHODS:The HSCs from rats were isolated and cultured in Dulbecco's Modified Eagle's Medium (DMEM) and treated with CAPE.The proliferation and collagen synthesis of HSCs were determined by ~3H-TdR and ~3H-proline incorporation respectively,and the expression of type Ⅰ,Ⅲ procollagen genes 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.CAPE also 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 increased from 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 collagen synthesis of HSC at lower concentration and induces HSC apoptosis at higher concentration.
基金
Natural Science Foundation of Yunnan Province for Younth,No.1999C0034Q,No.2000C0031Q