Flavonoids from tartary buckwheat induce G2/M cell cycle arrest and apoptosis in human hepatoma HepG2 cells
The cytotoxicity and antioxidant activity on human hepa toma cell line HepG2 of three flavonoids homogenous com pounds from tartary buckwheat seeds and bran, namely quercetin, isoquercetin, and rutin, were investigated. The total antioxidant competency detection results indicated that the antioxidan...
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| Veröffentlicht in: | Acta biochimica et biophysica Sinica 2014-06, Vol.46 (6), p.460-470 |
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| creator | Li, Yuying Duan, Shizhao Jia, Haiyan Bai, Chongzhi Zhang, Liwei Wang, Zhuanhua |
| description | The cytotoxicity and antioxidant activity on human hepa toma cell line HepG2 of three flavonoids homogenous com pounds from tartary buckwheat seeds and bran, namely quercetin, isoquercetin, and rutin, were investigated. The total antioxidant competency detection results indicated that the antioxidant capacity of quercetin was the strongest in a biological response system. A [3-（4,5-dimethylthiazol-2-yl）-2,5diphenyltetrazolium bromide] assay showed that quercetin exhibited the strongest cytotoxic effects against the HepG2 cell line. Flow cytometric analysis indicated that quercetin significantly increased the production of reactive oxygen species, and led to the G2/M phase arrest accom panied by an increase of apoptotic cell death after 48 h of incubation. Quercetininduced cell apoptosis was shown to involve p53 and p21 upregulation, Cyclin D1, Cdk2, and Cdk7 downregulation. These results suggested that the in duction of G2/M arrest, apoptosis, and cell death by quer cetin may associate with increased expression of p53 and p21, decrease of Cyclin D1, Cdk2, and Cdk7 levels, and generation of reactive oxygen species in cells. This study will help to better understand and fully utilize medicinal resources of plant flavonoids. |
| doi_str_mv | 10.1093/abbs/gmu023 |
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The total antioxidant competency detection results indicated that the antioxidant capacity of quercetin was the strongest in a biological response system. A [3-（4,5-dimethylthiazol-2-yl）-2,5diphenyltetrazolium bromide] assay showed that quercetin exhibited the strongest cytotoxic effects against the HepG2 cell line. Flow cytometric analysis indicated that quercetin significantly increased the production of reactive oxygen species, and led to the G2/M phase arrest accom panied by an increase of apoptotic cell death after 48 h of incubation. Quercetininduced cell apoptosis was shown to involve p53 and p21 upregulation, Cyclin D1, Cdk2, and Cdk7 downregulation. These results suggested that the in duction of G2/M arrest, apoptosis, and cell death by quer cetin may associate with increased expression of p53 and p21, decrease of Cyclin D1, Cdk2, and Cdk7 levels, and generation of reactive oxygen species in cells. This study will help to better understand and fully utilize medicinal resources of plant flavonoids.</description><identifier>ISSN: 1672-9145</identifier><identifier>EISSN: 1745-7270</identifier><identifier>DOI: 10.1093/abbs/gmu023</identifier><identifier>PMID: 24760952</identifier><language>eng</language><publisher>China</publisher><subject>Antioxidants - metabolism ; Apoptosis - drug effects ; Base Sequence ; Carcinoma, Hepatocellular - pathology ; Cell Division - drug effects ; Cell Line, Tumor ; DNA Primers ; Flavonoids - pharmacology ; Flow Cytometry ; G2 Phase - drug effects ; HepG2细胞 ; Humans ; Reactive Oxygen Species - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; 总抗氧化能力 ; 植物类黄酮 ; 细胞凋亡 ; 细胞周期阻滞 ; 细胞株 ; 苦荞</subject><ispartof>Acta biochimica et biophysica Sinica, 2014-06, Vol.46 (6), p.460-470</ispartof><rights>The Author 2014. 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The total antioxidant competency detection results indicated that the antioxidant capacity of quercetin was the strongest in a biological response system. A [3-（4,5-dimethylthiazol-2-yl）-2,5diphenyltetrazolium bromide] assay showed that quercetin exhibited the strongest cytotoxic effects against the HepG2 cell line. Flow cytometric analysis indicated that quercetin significantly increased the production of reactive oxygen species, and led to the G2/M phase arrest accom panied by an increase of apoptotic cell death after 48 h of incubation. Quercetininduced cell apoptosis was shown to involve p53 and p21 upregulation, Cyclin D1, Cdk2, and Cdk7 downregulation. These results suggested that the in duction of G2/M arrest, apoptosis, and cell death by quer cetin may associate with increased expression of p53 and p21, decrease of Cyclin D1, Cdk2, and Cdk7 levels, and generation of reactive oxygen species in cells. This study will help to better understand and fully utilize medicinal resources of plant flavonoids.</description><subject>Antioxidants - metabolism</subject><subject>Apoptosis - drug effects</subject><subject>Base Sequence</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell Division - drug effects</subject><subject>Cell Line, Tumor</subject><subject>DNA Primers</subject><subject>Flavonoids - pharmacology</subject><subject>Flow Cytometry</subject><subject>G2 Phase - drug effects</subject><subject>HepG2细胞</subject><subject>Humans</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>总抗氧化能力</subject><subject>植物类黄酮</subject><subject>细胞凋亡</subject><subject>细胞周期阻滞</subject><subject>细胞株</subject><subject>苦荞</subject><issn>1672-9145</issn><issn>1745-7270</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1PwzAMhiMEYuPjxB1FnLiUJc5Xe0QTDKQhLnCe3DTbCm3TNS1o_57ABlcky_bhsfX6NSEXnN1wlokJ5nmYrOqBgTggY26kSgwYdhh7bSDJuFQjchLCG2NCa86OyQik0SxTMCbv9xV--MaXRaDLzte0xy7GluaDff9cO-xp2RSDdXQGkydqXVVRu7WVo9h1LvQUm4Ji69vehzJElq6HGmN2Lfa-Rvrg2hn8zIUzcrTEKrjzfT0lr_d3L9OHZP48e5zezhPLU90nOs1AI1eQpoDMYCF4LpRTygoojDNMCtBgjUTMIF4ktETJ9TLT-VJzcOKUXO_2tp3fDFHkoi7DtwJsnB_CgqcgMqkzmf6PKsEEAGM8opd7dMhrVyzarqyjUYtfLyNwtQPs2jerTdms_hitIX6BMyW-AJiWf-A</recordid><startdate>201406</startdate><enddate>201406</enddate><creator>Li, Yuying</creator><creator>Duan, Shizhao</creator><creator>Jia, Haiyan</creator><creator>Bai, Chongzhi</creator><creator>Zhang, Liwei</creator><creator>Wang, Zhuanhua</creator><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W94</scope><scope>WU4</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>201406</creationdate><title>Flavonoids from tartary buckwheat induce G2/M cell cycle arrest and apoptosis in human hepatoma HepG2 cells</title><author>Li, Yuying ; 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The total antioxidant competency detection results indicated that the antioxidant capacity of quercetin was the strongest in a biological response system. A [3-（4,5-dimethylthiazol-2-yl）-2,5diphenyltetrazolium bromide] assay showed that quercetin exhibited the strongest cytotoxic effects against the HepG2 cell line. Flow cytometric analysis indicated that quercetin significantly increased the production of reactive oxygen species, and led to the G2/M phase arrest accom panied by an increase of apoptotic cell death after 48 h of incubation. Quercetininduced cell apoptosis was shown to involve p53 and p21 upregulation, Cyclin D1, Cdk2, and Cdk7 downregulation. These results suggested that the in duction of G2/M arrest, apoptosis, and cell death by quer cetin may associate with increased expression of p53 and p21, decrease of Cyclin D1, Cdk2, and Cdk7 levels, and generation of reactive oxygen species in cells. 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| subjects | Antioxidants - metabolism Apoptosis - drug effects Base Sequence Carcinoma, Hepatocellular - pathology Cell Division - drug effects Cell Line, Tumor DNA Primers Flavonoids - pharmacology Flow Cytometry G2 Phase - drug effects HepG2细胞 Humans Reactive Oxygen Species - metabolism Reverse Transcriptase Polymerase Chain Reaction 总抗氧化能力 植物类黄酮 细胞凋亡 细胞周期阻滞 细胞株 苦荞 |
| title | Flavonoids from tartary buckwheat induce G2/M cell cycle arrest and apoptosis in human hepatoma HepG2 cells |
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