2012•Chinese Journal of Clinical ResearchRequires access

The effect of arctigenin on proliferation and apoptosis of human esophageal cancer cells

Yao Yan-ju

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Abstract

Objective To evaluate the effect of arctigenin(ARG) on proliferation and apoptosis of human esophageal cancer-1(EC-1)cells and explore its mechanism.Methods The proliferation activity of EC-1 cells was detected by methylthiazol tetrazolium(MTT) method in ARG concentration of 2.5,5.0,10.0,20.0,40.0 mg/L and acting time of 24,48,72,96 and 120h.In ARG concentration of 10.0,20.0 and 40.0 mg/L and acting time of 24h,the apoptosis rate of EC-1 cells was assayed by flow cytometry(FCM),and the apoptotic index was respectively measured by agarose gel electrophoresis and TdT-mediated dUTP nick end labeling(TUNEL),and the expressions of apoptosis-related gene Bcl-2 and Bax were respectively detected by immunocytochemistry method.The impact of ARG of different concentration on EC-1 cells was analyzed.The negative control group without ARG was designed for serving as comparison.Results The proliferative activity of EC-1 cells can be inhibited by ARG in a dose/time dependent manner.The proliferation inhibitory rate of EC-1 cells was gradually increased in proportion to the increase of ARG concentration and active time(P0.05 or P0.01).The apoptotic rate and apoptotic index of EC-1 cells gradually increased,and the expression rate of Bcl-2 gradually decreased while the expression rate of Bax gradually increased in proportion to the increase of ARG concentration(all P0.01).There were significant differences on aforementioned changes compared with negative control group(P0.05 or P0.01).Conclusions ARG can inhibit the proliferation of EC-1 cells and induce apoptosis of EC-1 cells,and its mechanism may be associated with regulating expressions of Bcl-2 and Bax genes and thus inducing apoptosis of EC-1 cells.

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Objective To evaluate the effect of arctigenin(ARG) on proliferation and apoptosis of human esophageal cancer-1(EC-1)cells and explore its mechanism.Methods The proliferation activity of EC-1 cells was detected by methylthiazol tetrazolium(MTT) method in ARG concentration of 2.5,5.0,10.0,20.0,40.0 mg/L and acting time of 24,48,72,96 and 120h.In ARG concentration of 10.0,20.0 and 40.0 mg/L and acting time of 24h,the apoptosis rate of EC-1 cells was assayed by flow cytometry(FCM),and the apoptotic index was respectively measured by agarose gel electrophoresis and TdT-mediated dUTP nick end labeling(TUNEL),and the expressions of apoptosis-related gene Bcl-2 and Bax were respectively detected by immunocytochemistry method.The impact of ARG of different concentration on EC-1 cells was analyzed.The negative control group without ARG was designed for serving as comparison.Results The proliferative activity of EC-1 cells can be inhibited by ARG in a dose/time dependent manner.The proliferation inhibitory rate of EC-1 cells was gradually increased in proportion to the increase of ARG concentration and active time(P0.05 or P0.01).The apoptotic rate and apoptotic index of EC-1 cells gradually increased,and the expression rate of Bcl-2 gradually decreased while the expression rate of Bax gradually increased in proportion to the increase of ARG concentration(all P0.01).There were significant differences on aforementioned changes compared with negative control group(P0.05 or P0.01).Conclusions ARG can inhibit the proliferation of EC-1 cells and induce apoptosis of EC-1 cells,and its mechanism may be associated with regulating expressions of Bcl-2 and Bax genes and thus inducing apoptosis of EC-1 cells.

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Available abstract

Objective To evaluate the effect of arctigenin(ARG) on proliferation and apoptosis of human esophageal cancer-1(EC-1)cells and explore its mechanism.Methods The proliferation activity of EC-1 cells was detected by methylthiazol tetrazolium(MTT) method in ARG concentration of 2.5,5.0,10.0,20.0,40.0 mg/L and acting time of 24,48,72,96 and 120h.In ARG concentration of 10.0,20.0 and 40.0 mg/L and acting time of 24h,the apoptosis rate of EC-1 cells was assayed by flow cytometry(FCM),and the apoptotic index was respectively measured by agarose gel electrophoresis and TdT-mediated dUTP nick end labeling(TUNEL),and the expressions of apoptosis-related gene Bcl-2 and Bax were respectively detected by immunocytochemistry method.The impact of ARG of different concentration on EC-1 cells was analyzed.The negative control group without ARG was designed for serving as comparison.Results The proliferative activity of EC-1 cells can be inhibited by ARG in a dose/time dependent manner.The proliferation inhibitory rate of EC-1 cells was gradually increased in proportion to the increase of ARG concentration and active time(P0.05 or P0.01).The apoptotic rate and apoptotic index of EC-1 cells gradually increased,and the expression rate of Bcl-2 gradually decreased while the expression rate of Bax gradually increased in proportion to the increase of ARG concentration(all P0.01).There were significant differences on aforementioned changes compared with negative control group(P0.05 or P0.01).Conclusions ARG can inhibit the proliferation of EC-1 cells and induce apoptosis of EC-1 cells,and its mechanism may be associated with regulating expressions of Bcl-2 and Bax genes and thus inducing apoptosis of EC-1 cells.

Key concepts: Apoptosis, TUNEL assay, Flow cytometry, Molecular biology, Agarose gel electrophoresis, Immunocytochemistry, MTT assay, Proliferation index

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