The combination of baicalin and baicalein enhances apoptosis via the ERK/p38 MAPK pathway in human breast cancer cells
Aim： To examine whether the cell growth inhibitory effect of the combination of baicalin and baicalein is related to apoptosis. Moreover, to determine whether the expression of some apoptosis-related proteins is regulated by the ERK/p38 MAPK pathway. Methods： Cell viability was measured using a 3-（4...
Gespeichert in:
| Veröffentlicht in: | Acta pharmacologica Sinica 2009-12, Vol.30 (12), p.1648-1658 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1658 |
|---|---|
| container_issue | 12 |
| container_start_page | 1648 |
| container_title | Acta pharmacologica Sinica |
| container_volume | 30 |
| creator | Zhou, Qian-mei Wang, Song Zhang, Hui Lu, Yi-yu Wang, Xiu-feng Motoo, Yoshiharu Su, Shi-bing |
| description | Aim： To examine whether the cell growth inhibitory effect of the combination of baicalin and baicalein is related to apoptosis. Moreover, to determine whether the expression of some apoptosis-related proteins is regulated by the ERK/p38 MAPK pathway. Methods： Cell viability was measured using a 3-（4,5-dimethylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT） assay. Apoptosis was detected by acridine orange （AO） staining, DNA ladder assay and flow cytometric analysis. Apoptosis-related proteins were observed using Western blot analysis. Results： Compared with baicalin or baicalein alone, the combination treatment of baicalin （50 μmol/L） and baicalein （25 μmol/L） had an anti-proliferative effect in a time-dependent manner. Isobologram analysis demonstrated that the combination treatment had a synergistic effect. Moreover, apoptosis in MCF-7 cells was increased by 12% and 20% with the combination treatment at 24 h and 48 h, respectively. With the combination treatment in MCF-7 cells, cleaved caspase-3 and caspase-9 were observed, and the level of bcl-2 expression was decreased approximately 20% and 40% at 24 h and 48 h, respectively. The expression of bax and p53 were increased about 25% and 15% at 48 h, respectively. Moreover, the activation of caspase-3, -9 and the regulation of bcl-2, bax and p53 were related to ERK/p38 MAPK activation. Conclusion： In this study, apoptosis was enhanced by the combination treatment of baicalin and baicalein, which activated caspases-3 and caspase-9, downregulated the level of bcl-2 and upregulated the level of bax or p53 via the ERK/p38 MAPK pathway. |
| doi_str_mv | 10.1038/aps.2009.166 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4007493</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>32793735</cqvip_id><sourcerecordid>21369694</sourcerecordid><originalsourceid>FETCH-LOGICAL-c600t-8878f2713ee78d144646dfe75a981416c120d1811adf35adbb7292a24ac0a8a43</originalsourceid><addsrcrecordid>eNp9kt1r1jAUxosobk7vvJagoDf2Xb7aJDfCGPODTRSZ1-E0Td9mtknXtO_Yf7-UtzgV5lVyOL_znA-eLHtJ8IZgJo9hiBuKsdqQsnyUHRLBi1zQgj9O_1KQnGPJDrJnMV5hzCgj6ml2QJQqMSb4MNtdthaZ0FfOw-SCR6FBFTgDnfMIfL0GNkXWt-CNjQiGMEwhuoh2DtCUBM5-nB8PTKKvJ9_P0QBTewO3KJW0cw8eVaOFOCGzVI_I2K6Lz7MnDXTRvljfo-znx7PL08_5xbdPX05PLnKT5ptyKYVsqCDMWiFrwnnJy7qxogAlCSelIRTXRBICdcMKqKtKUEWBcjAYJHB2lH3Y6w5z1dvaWD-N0OlhdD2MtzqA039nvGv1Nuw0x1hwxZLAu1VgDNezjZPuXVxWAG_DHLVgaQxVKpzIt_8lKWELuMz05h_wKsyjT2fQjDAqcCH50vj1Q1RSwrSQhUjQ-z1kxhDjaJvfmxGsF3fo5A69uEMndyT81Z_XuIdXOyQg3wMxpfzWjvdNHxBchzRt8NvrVKIrML8a11mdNlFMsILdAWUgzrM</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>213025857</pqid></control><display><type>article</type><title>The combination of baicalin and baicalein enhances apoptosis via the ERK/p38 MAPK pathway in human breast cancer cells</title><source>MEDLINE</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><creator>Zhou, Qian-mei ; Wang, Song ; Zhang, Hui ; Lu, Yi-yu ; Wang, Xiu-feng ; Motoo, Yoshiharu ; Su, Shi-bing</creator><creatorcontrib>Zhou, Qian-mei ; Wang, Song ; Zhang, Hui ; Lu, Yi-yu ; Wang, Xiu-feng ; Motoo, Yoshiharu ; Su, Shi-bing</creatorcontrib><description>Aim： To examine whether the cell growth inhibitory effect of the combination of baicalin and baicalein is related to apoptosis. Moreover, to determine whether the expression of some apoptosis-related proteins is regulated by the ERK/p38 MAPK pathway. Methods： Cell viability was measured using a 3-（4,5-dimethylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT） assay. Apoptosis was detected by acridine orange （AO） staining, DNA ladder assay and flow cytometric analysis. Apoptosis-related proteins were observed using Western blot analysis. Results： Compared with baicalin or baicalein alone, the combination treatment of baicalin （50 μmol/L） and baicalein （25 μmol/L） had an anti-proliferative effect in a time-dependent manner. Isobologram analysis demonstrated that the combination treatment had a synergistic effect. Moreover, apoptosis in MCF-7 cells was increased by 12% and 20% with the combination treatment at 24 h and 48 h, respectively. With the combination treatment in MCF-7 cells, cleaved caspase-3 and caspase-9 were observed, and the level of bcl-2 expression was decreased approximately 20% and 40% at 24 h and 48 h, respectively. The expression of bax and p53 were increased about 25% and 15% at 48 h, respectively. Moreover, the activation of caspase-3, -9 and the regulation of bcl-2, bax and p53 were related to ERK/p38 MAPK activation. Conclusion： In this study, apoptosis was enhanced by the combination treatment of baicalin and baicalein, which activated caspases-3 and caspase-9, downregulated the level of bcl-2 and upregulated the level of bax or p53 via the ERK/p38 MAPK pathway.</description><identifier>ISSN: 1671-4083</identifier><identifier>ISSN: 1745-7254</identifier><identifier>EISSN: 1745-7254</identifier><identifier>DOI: 10.1038/aps.2009.166</identifier><identifier>PMID: 19960010</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Apoptosis ; Apoptosis - drug effects ; Baicalin ; BAX protein ; bax基因 ; Bcl-2 protein ; bcl-2-Associated X Protein - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Breast Neoplasms - drug therapy ; Breast Neoplasms - pathology ; caspase ; Caspase 3 - metabolism ; Caspase 9 - metabolism ; Caspase-3 ; Caspase-9 ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cell viability ; Drug Synergism ; Enzyme Inhibitors - pharmacology ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Female ; Flavanones - pharmacology ; Flavonoids - pharmacology ; Flow cytometry ; Humans ; Immunology ; Internal Medicine ; MAP kinase ; MAPK途径 ; Medical Microbiology ; Original ; original-article ; p38 Mitogen-Activated Protein Kinases - metabolism ; p53 Protein ; Pharmacology/Toxicology ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Tumor Suppressor Protein p53 - metabolism ; Vaccine ; 乳腺癌 ; 细胞凋亡 ; 黄芩素 ; 黄芩苷</subject><ispartof>Acta pharmacologica Sinica, 2009-12, Vol.30 (12), p.1648-1658</ispartof><rights>CPS and SIMM 2009</rights><rights>Copyright Nature Publishing Group Dec 2009</rights><rights>CPS and SIMM 2009.</rights><rights>Copyright © 2009 CPS and SIMM 2009 CPS and SIMM</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c600t-8878f2713ee78d144646dfe75a981416c120d1811adf35adbb7292a24ac0a8a43</citedby><cites>FETCH-LOGICAL-c600t-8878f2713ee78d144646dfe75a981416c120d1811adf35adbb7292a24ac0a8a43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/95561A/95561A.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007493/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007493/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19960010$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Qian-mei</creatorcontrib><creatorcontrib>Wang, Song</creatorcontrib><creatorcontrib>Zhang, Hui</creatorcontrib><creatorcontrib>Lu, Yi-yu</creatorcontrib><creatorcontrib>Wang, Xiu-feng</creatorcontrib><creatorcontrib>Motoo, Yoshiharu</creatorcontrib><creatorcontrib>Su, Shi-bing</creatorcontrib><title>The combination of baicalin and baicalein enhances apoptosis via the ERK/p38 MAPK pathway in human breast cancer cells</title><title>Acta pharmacologica Sinica</title><addtitle>Acta Pharmacol Sin</addtitle><addtitle>Acta Pharmacologica Sinica</addtitle><description>Aim： To examine whether the cell growth inhibitory effect of the combination of baicalin and baicalein is related to apoptosis. Moreover, to determine whether the expression of some apoptosis-related proteins is regulated by the ERK/p38 MAPK pathway. Methods： Cell viability was measured using a 3-（4,5-dimethylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT） assay. Apoptosis was detected by acridine orange （AO） staining, DNA ladder assay and flow cytometric analysis. Apoptosis-related proteins were observed using Western blot analysis. Results： Compared with baicalin or baicalein alone, the combination treatment of baicalin （50 μmol/L） and baicalein （25 μmol/L） had an anti-proliferative effect in a time-dependent manner. Isobologram analysis demonstrated that the combination treatment had a synergistic effect. Moreover, apoptosis in MCF-7 cells was increased by 12% and 20% with the combination treatment at 24 h and 48 h, respectively. With the combination treatment in MCF-7 cells, cleaved caspase-3 and caspase-9 were observed, and the level of bcl-2 expression was decreased approximately 20% and 40% at 24 h and 48 h, respectively. The expression of bax and p53 were increased about 25% and 15% at 48 h, respectively. Moreover, the activation of caspase-3, -9 and the regulation of bcl-2, bax and p53 were related to ERK/p38 MAPK activation. Conclusion： In this study, apoptosis was enhanced by the combination treatment of baicalin and baicalein, which activated caspases-3 and caspase-9, downregulated the level of bcl-2 and upregulated the level of bax or p53 via the ERK/p38 MAPK pathway.</description><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Baicalin</subject><subject>BAX protein</subject><subject>bax基因</subject><subject>Bcl-2 protein</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - pathology</subject><subject>caspase</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase 9 - metabolism</subject><subject>Caspase-3</subject><subject>Caspase-9</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cell viability</subject><subject>Drug Synergism</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Female</subject><subject>Flavanones - pharmacology</subject><subject>Flavonoids - pharmacology</subject><subject>Flow cytometry</subject><subject>Humans</subject><subject>Immunology</subject><subject>Internal Medicine</subject><subject>MAP kinase</subject><subject>MAPK途径</subject><subject>Medical Microbiology</subject><subject>Original</subject><subject>original-article</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>p53 Protein</subject><subject>Pharmacology/Toxicology</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Vaccine</subject><subject>乳腺癌</subject><subject>细胞凋亡</subject><subject>黄芩素</subject><subject>黄芩苷</subject><issn>1671-4083</issn><issn>1745-7254</issn><issn>1745-7254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kt1r1jAUxosobk7vvJagoDf2Xb7aJDfCGPODTRSZ1-E0Td9mtknXtO_Yf7-UtzgV5lVyOL_znA-eLHtJ8IZgJo9hiBuKsdqQsnyUHRLBi1zQgj9O_1KQnGPJDrJnMV5hzCgj6ml2QJQqMSb4MNtdthaZ0FfOw-SCR6FBFTgDnfMIfL0GNkXWt-CNjQiGMEwhuoh2DtCUBM5-nB8PTKKvJ9_P0QBTewO3KJW0cw8eVaOFOCGzVI_I2K6Lz7MnDXTRvljfo-znx7PL08_5xbdPX05PLnKT5ptyKYVsqCDMWiFrwnnJy7qxogAlCSelIRTXRBICdcMKqKtKUEWBcjAYJHB2lH3Y6w5z1dvaWD-N0OlhdD2MtzqA039nvGv1Nuw0x1hwxZLAu1VgDNezjZPuXVxWAG_DHLVgaQxVKpzIt_8lKWELuMz05h_wKsyjT2fQjDAqcCH50vj1Q1RSwrSQhUjQ-z1kxhDjaJvfmxGsF3fo5A69uEMndyT81Z_XuIdXOyQg3wMxpfzWjvdNHxBchzRt8NvrVKIrML8a11mdNlFMsILdAWUgzrM</recordid><startdate>20091201</startdate><enddate>20091201</enddate><creator>Zhou, Qian-mei</creator><creator>Wang, Song</creator><creator>Zhang, Hui</creator><creator>Lu, Yi-yu</creator><creator>Wang, Xiu-feng</creator><creator>Motoo, Yoshiharu</creator><creator>Su, Shi-bing</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><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>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20091201</creationdate><title>The combination of baicalin and baicalein enhances apoptosis via the ERK/p38 MAPK pathway in human breast cancer cells</title><author>Zhou, Qian-mei ; Wang, Song ; Zhang, Hui ; Lu, Yi-yu ; Wang, Xiu-feng ; Motoo, Yoshiharu ; Su, Shi-bing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c600t-8878f2713ee78d144646dfe75a981416c120d1811adf35adbb7292a24ac0a8a43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Baicalin</topic><topic>BAX protein</topic><topic>bax基因</topic><topic>Bcl-2 protein</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - pathology</topic><topic>caspase</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase 9 - metabolism</topic><topic>Caspase-3</topic><topic>Caspase-9</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cell viability</topic><topic>Drug Synergism</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Female</topic><topic>Flavanones - pharmacology</topic><topic>Flavonoids - pharmacology</topic><topic>Flow cytometry</topic><topic>Humans</topic><topic>Immunology</topic><topic>Internal Medicine</topic><topic>MAP kinase</topic><topic>MAPK途径</topic><topic>Medical Microbiology</topic><topic>Original</topic><topic>original-article</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>p53 Protein</topic><topic>Pharmacology/Toxicology</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Vaccine</topic><topic>乳腺癌</topic><topic>细胞凋亡</topic><topic>黄芩素</topic><topic>黄芩苷</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Qian-mei</creatorcontrib><creatorcontrib>Wang, Song</creatorcontrib><creatorcontrib>Zhang, Hui</creatorcontrib><creatorcontrib>Lu, Yi-yu</creatorcontrib><creatorcontrib>Wang, Xiu-feng</creatorcontrib><creatorcontrib>Motoo, Yoshiharu</creatorcontrib><creatorcontrib>Su, Shi-bing</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-自然科学</collection><collection>中文科技期刊数据库-自然科学-生物科学</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta pharmacologica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Qian-mei</au><au>Wang, Song</au><au>Zhang, Hui</au><au>Lu, Yi-yu</au><au>Wang, Xiu-feng</au><au>Motoo, Yoshiharu</au><au>Su, Shi-bing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The combination of baicalin and baicalein enhances apoptosis via the ERK/p38 MAPK pathway in human breast cancer cells</atitle><jtitle>Acta pharmacologica Sinica</jtitle><stitle>Acta Pharmacol Sin</stitle><addtitle>Acta Pharmacologica Sinica</addtitle><date>2009-12-01</date><risdate>2009</risdate><volume>30</volume><issue>12</issue><spage>1648</spage><epage>1658</epage><pages>1648-1658</pages><issn>1671-4083</issn><issn>1745-7254</issn><eissn>1745-7254</eissn><abstract>Aim： To examine whether the cell growth inhibitory effect of the combination of baicalin and baicalein is related to apoptosis. Moreover, to determine whether the expression of some apoptosis-related proteins is regulated by the ERK/p38 MAPK pathway. Methods： Cell viability was measured using a 3-（4,5-dimethylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT） assay. Apoptosis was detected by acridine orange （AO） staining, DNA ladder assay and flow cytometric analysis. Apoptosis-related proteins were observed using Western blot analysis. Results： Compared with baicalin or baicalein alone, the combination treatment of baicalin （50 μmol/L） and baicalein （25 μmol/L） had an anti-proliferative effect in a time-dependent manner. Isobologram analysis demonstrated that the combination treatment had a synergistic effect. Moreover, apoptosis in MCF-7 cells was increased by 12% and 20% with the combination treatment at 24 h and 48 h, respectively. With the combination treatment in MCF-7 cells, cleaved caspase-3 and caspase-9 were observed, and the level of bcl-2 expression was decreased approximately 20% and 40% at 24 h and 48 h, respectively. The expression of bax and p53 were increased about 25% and 15% at 48 h, respectively. Moreover, the activation of caspase-3, -9 and the regulation of bcl-2, bax and p53 were related to ERK/p38 MAPK activation. Conclusion： In this study, apoptosis was enhanced by the combination treatment of baicalin and baicalein, which activated caspases-3 and caspase-9, downregulated the level of bcl-2 and upregulated the level of bax or p53 via the ERK/p38 MAPK pathway.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>19960010</pmid><doi>10.1038/aps.2009.166</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1671-4083 |
| ispartof | Acta pharmacologica Sinica, 2009-12, Vol.30 (12), p.1648-1658 |
| issn | 1671-4083 1745-7254 1745-7254 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4007493 |
| source | MEDLINE; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | Apoptosis Apoptosis - drug effects Baicalin BAX protein bax基因 Bcl-2 protein bcl-2-Associated X Protein - metabolism Biomedical and Life Sciences Biomedicine Breast Neoplasms - drug therapy Breast Neoplasms - pathology caspase Caspase 3 - metabolism Caspase 9 - metabolism Caspase-3 Caspase-9 Cell Line, Tumor Cell Proliferation - drug effects Cell Survival - drug effects Cell viability Drug Synergism Enzyme Inhibitors - pharmacology Extracellular Signal-Regulated MAP Kinases - metabolism Female Flavanones - pharmacology Flavonoids - pharmacology Flow cytometry Humans Immunology Internal Medicine MAP kinase MAPK途径 Medical Microbiology Original original-article p38 Mitogen-Activated Protein Kinases - metabolism p53 Protein Pharmacology/Toxicology Proto-Oncogene Proteins c-bcl-2 - metabolism Signal Transduction - drug effects Signal Transduction - physiology Tumor Suppressor Protein p53 - metabolism Vaccine 乳腺癌 细胞凋亡 黄芩素 黄芩苷 |
| title | The combination of baicalin and baicalein enhances apoptosis via the ERK/p38 MAPK pathway in human breast cancer cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T13%3A14%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20combination%20of%20baicalin%20and%20baicalein%20enhances%20apoptosis%20via%20the%20ERK/p38%20MAPK%20pathway%20in%20human%20breast%20cancer%20cells&rft.jtitle=Acta%20pharmacologica%20Sinica&rft.au=Zhou,%20Qian-mei&rft.date=2009-12-01&rft.volume=30&rft.issue=12&rft.spage=1648&rft.epage=1658&rft.pages=1648-1658&rft.issn=1671-4083&rft.eissn=1745-7254&rft_id=info:doi/10.1038/aps.2009.166&rft_dat=%3Cproquest_pubme%3E21369694%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=213025857&rft_id=info:pmid/19960010&rft_cqvip_id=32793735&rfr_iscdi=true |