Effect of atractylone on the viability and apoptosis of hepatoma HepG2 cells and related mechanism
ObjectiveTo investigate the effect of atractylone on the viability and apoptosis of hepatoma HepG2 cells and its mechanism of action. MethodsHepatoma HepG2 cells were selected and divided into low-, middle-, and high-dose atractylone groups (5, 10, and 20 μmol/L), and the cells in the control group...
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Editorial Department of Journal of Clinical Hepatology
2021
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oai:doaj.org-article:146858d810a9433fbb2880e8166009fa2021-11-17T10:57:57ZEffect of atractylone on the viability and apoptosis of hepatoma HepG2 cells and related mechanism1001-5256https://doaj.org/article/146858d810a9433fbb2880e8166009fa2021-11-01T00:00:00Zhttp://www.lcgdbzz.org/cn/article/doi/10.3969/j.issn.1001-5256.2021.11.020https://doaj.org/toc/1001-5256ObjectiveTo investigate the effect of atractylone on the viability and apoptosis of hepatoma HepG2 cells and its mechanism of action. MethodsHepatoma HepG2 cells were selected and divided into low-, middle-, and high-dose atractylone groups (5, 10, and 20 μmol/L), and the cells in the control group were added with an equal volume of DMSO. MTT colorimetry was used to measure the viability of HepG2 cells after treatment with different concentrations of atractylone; flow cytometry was used to measure the apoptosis rate and mitochondrial membrane potential of HepG2 cells; the DCFH-DA fluorescent probe labeling method was used to measure the level of reactive oxygen species (ROS) in HepG2 cells; Transwell assay was used to evaluate the effect of atractylone on the migration ability of HepG2 cells; Western blot was used to measure the protein expression levels of Bcl-2, Bax, and cleaved caspase-3. A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for comparison between two groups. ResultsAfter 24 and 48 hours of treatment with atractylone, compared with the control group, the low-, middle-, and high-dose atractylone groups had a tendency of reduction in cell viability (all P<0.05), with a half inhibitory concentration of 26.19 μmol/L in atractylone treatment of HepG2 cells for 72 hours. The low-, middle-, and high-dose atractylone groups had a significantly higher apoptosis rate than the control group (14.34%/29.32%/50.12% vs 0.32%, all P<0.05). Compared with the control group, the low-, middle-, and high-dose atractylone groups had a significant increase in the fluorescence intensity of ROS in HepG2 cells (all P<0.05). After 48 hours of treatment with atractylone, compared with the control group, the low-, middle-, and high-dose atractylone groups had a significant reduction in the number of migrated cells (132.67±18.36/57.00±9.26/31.00±2.45 vs 258.11±38.54, P<0.05). Compared with the control group, the low-, middle-, and high-dose atractylone groups had a significant reduction in the expression of the anti-apoptotic factor Bcl-2 and significant increases in the expression of the apoptotic factors Bax and cleaved caspase-3 (all P<0.05). ConclusionAtractylone can induce the apoptosis and inhibit the migration of HepG2 cells, which provides an experimental basis for further development and utilization of atractylone.YANG XueliEditorial Department of Journal of Clinical HepatologyarticleDiseases of the digestive system. GastroenterologyRC799-869ZHLinchuang Gandanbing Zazhi, Vol 37, Iss 11, Pp 2589-2594 (2021) |
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Diseases of the digestive system. Gastroenterology RC799-869 |
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Diseases of the digestive system. Gastroenterology RC799-869 YANG Xueli Effect of atractylone on the viability and apoptosis of hepatoma HepG2 cells and related mechanism |
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ObjectiveTo investigate the effect of atractylone on the viability and apoptosis of hepatoma HepG2 cells and its mechanism of action. MethodsHepatoma HepG2 cells were selected and divided into low-, middle-, and high-dose atractylone groups (5, 10, and 20 μmol/L), and the cells in the control group were added with an equal volume of DMSO. MTT colorimetry was used to measure the viability of HepG2 cells after treatment with different concentrations of atractylone; flow cytometry was used to measure the apoptosis rate and mitochondrial membrane potential of HepG2 cells; the DCFH-DA fluorescent probe labeling method was used to measure the level of reactive oxygen species (ROS) in HepG2 cells; Transwell assay was used to evaluate the effect of atractylone on the migration ability of HepG2 cells; Western blot was used to measure the protein expression levels of Bcl-2, Bax, and cleaved caspase-3. A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for comparison between two groups. ResultsAfter 24 and 48 hours of treatment with atractylone, compared with the control group, the low-, middle-, and high-dose atractylone groups had a tendency of reduction in cell viability (all P<0.05), with a half inhibitory concentration of 26.19 μmol/L in atractylone treatment of HepG2 cells for 72 hours. The low-, middle-, and high-dose atractylone groups had a significantly higher apoptosis rate than the control group (14.34%/29.32%/50.12% vs 0.32%, all P<0.05). Compared with the control group, the low-, middle-, and high-dose atractylone groups had a significant increase in the fluorescence intensity of ROS in HepG2 cells (all P<0.05). After 48 hours of treatment with atractylone, compared with the control group, the low-, middle-, and high-dose atractylone groups had a significant reduction in the number of migrated cells (132.67±18.36/57.00±9.26/31.00±2.45 vs 258.11±38.54, P<0.05). Compared with the control group, the low-, middle-, and high-dose atractylone groups had a significant reduction in the expression of the anti-apoptotic factor Bcl-2 and significant increases in the expression of the apoptotic factors Bax and cleaved caspase-3 (all P<0.05). ConclusionAtractylone can induce the apoptosis and inhibit the migration of HepG2 cells, which provides an experimental basis for further development and utilization of atractylone. |
format |
article |
author |
YANG Xueli |
author_facet |
YANG Xueli |
author_sort |
YANG Xueli |
title |
Effect of atractylone on the viability and apoptosis of hepatoma HepG2 cells and related mechanism |
title_short |
Effect of atractylone on the viability and apoptosis of hepatoma HepG2 cells and related mechanism |
title_full |
Effect of atractylone on the viability and apoptosis of hepatoma HepG2 cells and related mechanism |
title_fullStr |
Effect of atractylone on the viability and apoptosis of hepatoma HepG2 cells and related mechanism |
title_full_unstemmed |
Effect of atractylone on the viability and apoptosis of hepatoma HepG2 cells and related mechanism |
title_sort |
effect of atractylone on the viability and apoptosis of hepatoma hepg2 cells and related mechanism |
publisher |
Editorial Department of Journal of Clinical Hepatology |
publishDate |
2021 |
url |
https://doaj.org/article/146858d810a9433fbb2880e8166009fa |
work_keys_str_mv |
AT yangxueli effectofatractyloneontheviabilityandapoptosisofhepatomahepg2cellsandrelatedmechanism |
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1718425591927013376 |