Activation of AMPK by Buddleja officinalis Maxim. Flower Extract Contributes to Protecting Hepatocytes from Oxidative Stress
The Buddleja officinalis Maxim. flower is used in traditional Chinese and Korean medicine to treat inflammation, vascular diseases, headache, and stroke, as well as enhance liver function. This research investigated the effects of B. officinalis Maxim. flower extract (BFE) on hepatotoxicity. The cyt...
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| Veröffentlicht in: | Evidence-based complementary and alternative medicine 2017-01, Vol.2017 (2017), p.1-15 |
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| creator | Ku, Sae-Kwang Zhao, RongJie Kim, Sang Chan Jung, Dae Hwa Cho, Il Je Park, Chung A. Kim, Jae Kwang Jegal, Kyung Hwan Park, Sang Mi Lee, Chul Won Jung, Ji Yun An, Won G. |
| description | The Buddleja officinalis Maxim. flower is used in traditional Chinese and Korean medicine to treat inflammation, vascular diseases, headache, and stroke, as well as enhance liver function. This research investigated the effects of B. officinalis Maxim. flower extract (BFE) on hepatotoxicity. The cytoprotective effects and mechanism of BFE against severe mitochondrial dysfunction and H2O2 production in hepatotoxicity induced by coadministration of arachidonic acid (AA) and iron were observed in the HepG2 cell line. In addition, we performed blood biochemical, histopathological, and histomorphometric analyses of mice with carbon tetrachloride- (CCl4-) induced acute liver damage. BFE inhibited the AA + iron-mediated hepatotoxicity of HepG2 cells. Moreover, it inhibited mitochondrial dysfunction, H2O2 production, and glutathione depletion mediated by AA + iron in the same cells. Meanwhile, the cytoprotective effects of BFE against oxidative stress were associated with the activation of AMP-activated protein kinase (AMPK). In particular, based on the histopathological observations, BFE (30 and 100 mg/kg) showed clear hepatoprotective effects against CCl4-induced acute hepatic damage. Furthermore, it inhibited 4-hydroxynonenal and nitrotyrosine immunoreactivity in hepatocytes. These results provide evidence that BFE has beneficial hepatoprotective effects against hepatic damage via the activation of AMPK pathway. Accordingly, BFE may have therapeutic potential for diverse liver disorders. |
| doi_str_mv | 10.1155/2017/9253462 |
| format | Article |
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Flower Extract Contributes to Protecting Hepatocytes from Oxidative Stress</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central Open Access</source><source>Wiley-Blackwell Open Access Titles</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Ku, Sae-Kwang ; Zhao, RongJie ; Kim, Sang Chan ; Jung, Dae Hwa ; Cho, Il Je ; Park, Chung A. ; Kim, Jae Kwang ; Jegal, Kyung Hwan ; Park, Sang Mi ; Lee, Chul Won ; Jung, Ji Yun ; An, Won G.</creator><contributor>Cuman, Roberto K. N.</contributor><creatorcontrib>Ku, Sae-Kwang ; Zhao, RongJie ; Kim, Sang Chan ; Jung, Dae Hwa ; Cho, Il Je ; Park, Chung A. ; Kim, Jae Kwang ; Jegal, Kyung Hwan ; Park, Sang Mi ; Lee, Chul Won ; Jung, Ji Yun ; An, Won G. ; Cuman, Roberto K. N.</creatorcontrib><description>The Buddleja officinalis Maxim. flower is used in traditional Chinese and Korean medicine to treat inflammation, vascular diseases, headache, and stroke, as well as enhance liver function. This research investigated the effects of B. officinalis Maxim. flower extract (BFE) on hepatotoxicity. The cytoprotective effects and mechanism of BFE against severe mitochondrial dysfunction and H2O2 production in hepatotoxicity induced by coadministration of arachidonic acid (AA) and iron were observed in the HepG2 cell line. In addition, we performed blood biochemical, histopathological, and histomorphometric analyses of mice with carbon tetrachloride- (CCl4-) induced acute liver damage. BFE inhibited the AA + iron-mediated hepatotoxicity of HepG2 cells. Moreover, it inhibited mitochondrial dysfunction, H2O2 production, and glutathione depletion mediated by AA + iron in the same cells. Meanwhile, the cytoprotective effects of BFE against oxidative stress were associated with the activation of AMP-activated protein kinase (AMPK). In particular, based on the histopathological observations, BFE (30 and 100 mg/kg) showed clear hepatoprotective effects against CCl4-induced acute hepatic damage. Furthermore, it inhibited 4-hydroxynonenal and nitrotyrosine immunoreactivity in hepatocytes. These results provide evidence that BFE has beneficial hepatoprotective effects against hepatic damage via the activation of AMPK pathway. Accordingly, BFE may have therapeutic potential for diverse liver disorders.</description><identifier>ISSN: 1741-427X</identifier><identifier>EISSN: 1741-4288</identifier><identifier>DOI: 10.1155/2017/9253462</identifier><identifier>PMID: 28473864</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Apoptosis ; Arachidonic acid ; Carbon tetrachloride ; Chromatography ; Colleges & universities ; Fatty acids ; Flavonoids ; Kinases ; Liver diseases ; Medicine ; Oxidative stress ; Polyclonal antibodies ; Rodents ; Sensors ; Variance analysis</subject><ispartof>Evidence-based complementary and alternative medicine, 2017-01, Vol.2017 (2017), p.1-15</ispartof><rights>Copyright © 2017 Ji Yun Jung et al.</rights><rights>COPYRIGHT 2017 John Wiley & Sons, Inc.</rights><rights>Copyright © 2017 Ji Yun Jung et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2017 Ji Yun Jung et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-abddc34ff5242ebf12ef93afe047cd4f9c7348b3331e10fc017e424bbedae15d3</citedby><cites>FETCH-LOGICAL-c499t-abddc34ff5242ebf12ef93afe047cd4f9c7348b3331e10fc017e424bbedae15d3</cites><orcidid>0000-0002-1341-2114 ; 0000-0001-6295-0608 ; 0000-0002-4899-672X ; 0000-0003-3845-6268 ; 0000-0002-7781-1480 ; 0000-0003-0515-0764</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5394415/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5394415/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28473864$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Cuman, Roberto K. N.</contributor><creatorcontrib>Ku, Sae-Kwang</creatorcontrib><creatorcontrib>Zhao, RongJie</creatorcontrib><creatorcontrib>Kim, Sang Chan</creatorcontrib><creatorcontrib>Jung, Dae Hwa</creatorcontrib><creatorcontrib>Cho, Il Je</creatorcontrib><creatorcontrib>Park, Chung A.</creatorcontrib><creatorcontrib>Kim, Jae Kwang</creatorcontrib><creatorcontrib>Jegal, Kyung Hwan</creatorcontrib><creatorcontrib>Park, Sang Mi</creatorcontrib><creatorcontrib>Lee, Chul Won</creatorcontrib><creatorcontrib>Jung, Ji Yun</creatorcontrib><creatorcontrib>An, Won G.</creatorcontrib><title>Activation of AMPK by Buddleja officinalis Maxim. Flower Extract Contributes to Protecting Hepatocytes from Oxidative Stress</title><title>Evidence-based complementary and alternative medicine</title><addtitle>Evid Based Complement Alternat Med</addtitle><description>The Buddleja officinalis Maxim. flower is used in traditional Chinese and Korean medicine to treat inflammation, vascular diseases, headache, and stroke, as well as enhance liver function. This research investigated the effects of B. officinalis Maxim. flower extract (BFE) on hepatotoxicity. The cytoprotective effects and mechanism of BFE against severe mitochondrial dysfunction and H2O2 production in hepatotoxicity induced by coadministration of arachidonic acid (AA) and iron were observed in the HepG2 cell line. In addition, we performed blood biochemical, histopathological, and histomorphometric analyses of mice with carbon tetrachloride- (CCl4-) induced acute liver damage. BFE inhibited the AA + iron-mediated hepatotoxicity of HepG2 cells. Moreover, it inhibited mitochondrial dysfunction, H2O2 production, and glutathione depletion mediated by AA + iron in the same cells. Meanwhile, the cytoprotective effects of BFE against oxidative stress were associated with the activation of AMP-activated protein kinase (AMPK). In particular, based on the histopathological observations, BFE (30 and 100 mg/kg) showed clear hepatoprotective effects against CCl4-induced acute hepatic damage. Furthermore, it inhibited 4-hydroxynonenal and nitrotyrosine immunoreactivity in hepatocytes. These results provide evidence that BFE has beneficial hepatoprotective effects against hepatic damage via the activation of AMPK pathway. Accordingly, BFE may have therapeutic potential for diverse liver disorders.</description><subject>Apoptosis</subject><subject>Arachidonic acid</subject><subject>Carbon tetrachloride</subject><subject>Chromatography</subject><subject>Colleges & universities</subject><subject>Fatty acids</subject><subject>Flavonoids</subject><subject>Kinases</subject><subject>Liver diseases</subject><subject>Medicine</subject><subject>Oxidative stress</subject><subject>Polyclonal antibodies</subject><subject>Rodents</subject><subject>Sensors</subject><subject>Variance analysis</subject><issn>1741-427X</issn><issn>1741-4288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkc9rFDEUxwdRbK3ePEvAi6DbTn5NJhdhXVortrSggreQybxss8xO1iSz3QX_eDPsulVPnhLyPnzy3vsWxUtcnmLM-RkpsTiThFNWkUfFMRYMTxip68eHu_h-VDyLcVGWRAohnhZHpGaC1hU7Ln5OTXJrnZzvkbdoen37GTVb9GFo2w4WOr9ZZ1yvOxfRtd645Sm66Pw9BHS-SUGbhGa-T8E1Q4KIkke3wSfIzn6OLmGlkzfbsWKDX6KbjWvzV2tAX1KAGJ8XT6zuIrzYnyfFt4vzr7PLydXNx0-z6dXEMCnTRDdtayizlhNGoLGYgJVUWyiZMC2z0gjK6oZSigGX1uSFACOsaaDVgHlLT4r3O-9qaJbQGsgd606tglvqsFVeO_V3pXd3au7XilPJGOZZ8GYvCP7HADGppYsGuk734IeocC2rkuFS4oy-_gdd-CHkBY5ULWnFBCcP1Fx3oFxv_bjMUaqmnFdlxSohM_VuR5ngYwxgDy3jUo3hqzF8tQ8_46_-HPMA_047A293wJ3rW33v_lMHmQGrH2jMmeSY_gL_KsKd</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Ku, Sae-Kwang</creator><creator>Zhao, RongJie</creator><creator>Kim, Sang Chan</creator><creator>Jung, Dae Hwa</creator><creator>Cho, Il Je</creator><creator>Park, Chung A.</creator><creator>Kim, Jae Kwang</creator><creator>Jegal, Kyung Hwan</creator><creator>Park, Sang Mi</creator><creator>Lee, Chul Won</creator><creator>Jung, Ji Yun</creator><creator>An, Won G.</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M2M</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1341-2114</orcidid><orcidid>https://orcid.org/0000-0001-6295-0608</orcidid><orcidid>https://orcid.org/0000-0002-4899-672X</orcidid><orcidid>https://orcid.org/0000-0003-3845-6268</orcidid><orcidid>https://orcid.org/0000-0002-7781-1480</orcidid><orcidid>https://orcid.org/0000-0003-0515-0764</orcidid></search><sort><creationdate>20170101</creationdate><title>Activation of AMPK by Buddleja officinalis Maxim. 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N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of AMPK by Buddleja officinalis Maxim. Flower Extract Contributes to Protecting Hepatocytes from Oxidative Stress</atitle><jtitle>Evidence-based complementary and alternative medicine</jtitle><addtitle>Evid Based Complement Alternat Med</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>2017</volume><issue>2017</issue><spage>1</spage><epage>15</epage><pages>1-15</pages><issn>1741-427X</issn><eissn>1741-4288</eissn><abstract>The Buddleja officinalis Maxim. flower is used in traditional Chinese and Korean medicine to treat inflammation, vascular diseases, headache, and stroke, as well as enhance liver function. This research investigated the effects of B. officinalis Maxim. flower extract (BFE) on hepatotoxicity. The cytoprotective effects and mechanism of BFE against severe mitochondrial dysfunction and H2O2 production in hepatotoxicity induced by coadministration of arachidonic acid (AA) and iron were observed in the HepG2 cell line. In addition, we performed blood biochemical, histopathological, and histomorphometric analyses of mice with carbon tetrachloride- (CCl4-) induced acute liver damage. BFE inhibited the AA + iron-mediated hepatotoxicity of HepG2 cells. Moreover, it inhibited mitochondrial dysfunction, H2O2 production, and glutathione depletion mediated by AA + iron in the same cells. Meanwhile, the cytoprotective effects of BFE against oxidative stress were associated with the activation of AMP-activated protein kinase (AMPK). In particular, based on the histopathological observations, BFE (30 and 100 mg/kg) showed clear hepatoprotective effects against CCl4-induced acute hepatic damage. Furthermore, it inhibited 4-hydroxynonenal and nitrotyrosine immunoreactivity in hepatocytes. These results provide evidence that BFE has beneficial hepatoprotective effects against hepatic damage via the activation of AMPK pathway. Accordingly, BFE may have therapeutic potential for diverse liver disorders.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>28473864</pmid><doi>10.1155/2017/9253462</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-1341-2114</orcidid><orcidid>https://orcid.org/0000-0001-6295-0608</orcidid><orcidid>https://orcid.org/0000-0002-4899-672X</orcidid><orcidid>https://orcid.org/0000-0003-3845-6268</orcidid><orcidid>https://orcid.org/0000-0002-7781-1480</orcidid><orcidid>https://orcid.org/0000-0003-0515-0764</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Wiley-Blackwell Open Access Titles; PubMed Central; Alma/SFX Local Collection |
| subjects | Apoptosis Arachidonic acid Carbon tetrachloride Chromatography Colleges & universities Fatty acids Flavonoids Kinases Liver diseases Medicine Oxidative stress Polyclonal antibodies Rodents Sensors Variance analysis |
| title | Activation of AMPK by Buddleja officinalis Maxim. Flower Extract Contributes to Protecting Hepatocytes from Oxidative Stress |
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