TY - JOUR
T1 - The Chinese medicine Bu-Zhong-Yi-Qi-Tang inhibited proliferation of hepatoma cell lines by inducing apoptosis via G0/G1 arrest
AU - Kao, Shung Te
AU - Yeh, Chia Chou
AU - Hsieh, Chang Chi
AU - Yang, Mei Do
AU - Lee, Miau Rong
AU - Liu, Hsiao Sheng
AU - Lin, Jaung Geng
N1 - Funding Information:
This study was supported by the Supervisory Committee for the Integration of Western and Chinese Medicine (SCIWCM86C-004; SCIWCM86C-007), and Chinese Medical college (CMC88-PCM-01). We appreciate Dr. Hsu S.L. for kindly gift of HepG2 and Hep3B cell lines.
PY - 2001/8/17
Y1 - 2001/8/17
N2 - Bu-Zhong-Yi-Qi-Tang (BZYQT), a Chinese herbal medicine, inhibited the proliferation of human hepatoma cell lines (Hep3B, HepG2 and HA22T) dose-dependently. The IC50s of BZYQT on the proliferation of Hep3B, HepG2 and HA22T were 432.5±31.8 μg/ml, 455.4±24.2 μg/ml, and 2284.3±77.2 μg/ml respectively on day 3. However, BZYQT did not significantly inhibit the proliferation of normal human hepatocytes (Chang liver, CCL-13) at the concentration under 5,000μg/ml. Major compounds of BZYQT, including astragaloside IV, ginsenoside Rb1 and Rg1, saikosaponin a and c, and glycyrrhizin, have been identified. To investigate the key inhibitors of BZYQT, Hep3B cells were treated with BZYQT, individual major compounds of BZYQT, and mixture of major compounds in the same ratio as present in BZYQT. Significant inhibition of proliferation was detected in BZYQT and its major compounds mixture in a comparable level. Not any individual major compound examined could suppress the proliferation of Hep3B cells. This data indicated that there could be synergistic or additive effects of the ingredients in BZYQT. BrdU incorporation, cell cycle analysis and DNA fragmentation assay revealed that BZYQT suppressed the proliferation of hepatoma cells via G0/G1 cell cycle arrest and inhibition of DNA synthesis followed by apoptosis.
AB - Bu-Zhong-Yi-Qi-Tang (BZYQT), a Chinese herbal medicine, inhibited the proliferation of human hepatoma cell lines (Hep3B, HepG2 and HA22T) dose-dependently. The IC50s of BZYQT on the proliferation of Hep3B, HepG2 and HA22T were 432.5±31.8 μg/ml, 455.4±24.2 μg/ml, and 2284.3±77.2 μg/ml respectively on day 3. However, BZYQT did not significantly inhibit the proliferation of normal human hepatocytes (Chang liver, CCL-13) at the concentration under 5,000μg/ml. Major compounds of BZYQT, including astragaloside IV, ginsenoside Rb1 and Rg1, saikosaponin a and c, and glycyrrhizin, have been identified. To investigate the key inhibitors of BZYQT, Hep3B cells were treated with BZYQT, individual major compounds of BZYQT, and mixture of major compounds in the same ratio as present in BZYQT. Significant inhibition of proliferation was detected in BZYQT and its major compounds mixture in a comparable level. Not any individual major compound examined could suppress the proliferation of Hep3B cells. This data indicated that there could be synergistic or additive effects of the ingredients in BZYQT. BrdU incorporation, cell cycle analysis and DNA fragmentation assay revealed that BZYQT suppressed the proliferation of hepatoma cells via G0/G1 cell cycle arrest and inhibition of DNA synthesis followed by apoptosis.
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U2 - 10.1016/S0024-3205(01)01226-7
DO - 10.1016/S0024-3205(01)01226-7
M3 - Article
C2 - 11554610
AN - SCOPUS:0035902794
VL - 69
SP - 1485
EP - 1496
JO - Life Sciences
JF - Life Sciences
SN - 0024-3205
IS - 13
ER -
