2011Clinical Education of General PracticeRequires access

Influence of arsenic trioxide on apoptosis and Bcl-2/Bax expression of hepatoma cell line HepG2

Jiang Pingli

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Abstract

Objective To investigate the apoptosis inducing activity of arsenic trioxide in hepatoma cell line HepG2 and its mechanisms.Methods HepG2 cells were treated with arsenic trioxide at 1.25,2.5,5,10,20μmol/L.Cell growth inhibitory rate was detected by MTT colorimetric assay every 24 hours.Apoptosis rate was analyzed by Annexin V/PI fluorescence staining and TUNEL.Changes in expression of Bcl-2 and Bax protein were assayed by flow cytometry.Results MTT tests showed HepG2 cell proliferation was significantly inhibited by arsenic trioxide in time and dosedependent fashion.Marked apoptosis was detected by Annexin V/PI and TUNEL in HepG2 cells after treatment by arsenic trioxide at 5,10,20μmol/L after 24 hours and increased in a dose-dependent manner(t=-2.96,-4.15,-7.33,P 0.05).The Bcl-2 expression decreased and the Bax expression increased in HepG2 cells induced by arsenic trioxide after 24 hours (t=3.59,5.65,6.94,7.62,7.92,P0.05).Conclusions Bcl-2 and Bax protein probably correlated with the activation of apoptosis in HepG2 cells induced by arsenic trioxide.

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Objective To investigate the apoptosis inducing activity of arsenic trioxide in hepatoma cell line HepG2 and its mechanisms.Methods HepG2 cells were treated with arsenic trioxide at 1.25,2.5,5,10,20μmol/L.Cell growth inhibitory rate was detected by MTT colorimetric assay every 24 hours.Apoptosis rate was analyzed by Annexin V/PI fluorescence staining and TUNEL.Changes in expression of Bcl-2 and Bax protein were assayed by flow cytometry.Results MTT tests showed HepG2 cell proliferation was significantly inhibited by arsenic trioxide in time and dosedependent fashion.Marked apoptosis was detected by Annexin V/PI and TUNEL in HepG2 cells after treatment by arsenic trioxide at 5,10,20μmol/L after 24 hours and increased in a dose-dependent manner(t=-2.96,-4.15,-7.33,P 0.05).The Bcl-2 expression decreased and the Bax expression increased in HepG2 cells induced by arsenic trioxide after 24 hours (t=3.59,5.65,6.94,7.62,7.92,P0.05).Conclusions Bcl-2 and Bax protein probably correlated with the activation of apoptosis in HepG2 cells induced by arsenic trioxide.

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Available abstract

Objective To investigate the apoptosis inducing activity of arsenic trioxide in hepatoma cell line HepG2 and its mechanisms.Methods HepG2 cells were treated with arsenic trioxide at 1.25,2.5,5,10,20μmol/L.Cell growth inhibitory rate was detected by MTT colorimetric assay every 24 hours.Apoptosis rate was analyzed by Annexin V/PI fluorescence staining and TUNEL.Changes in expression of Bcl-2 and Bax protein were assayed by flow cytometry.Results MTT tests showed HepG2 cell proliferation was significantly inhibited by arsenic trioxide in time and dosedependent fashion.Marked apoptosis was detected by Annexin V/PI and TUNEL in HepG2 cells after treatment by arsenic trioxide at 5,10,20μmol/L after 24 hours and increased in a dose-dependent manner(t=-2.96,-4.15,-7.33,P 0.05).The Bcl-2 expression decreased and the Bax expression increased in HepG2 cells induced by arsenic trioxide after 24 hours (t=3.59,5.65,6.94,7.62,7.92,P0.05).Conclusions Bcl-2 and Bax protein probably correlated with the activation of apoptosis in HepG2 cells induced by arsenic trioxide.

Key concepts: Arsenic trioxide, Apoptosis, Annexin, TUNEL assay, MTT assay, Flow cytometry, Molecular biology, Arsenic

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