Protocatechuic acid inhibits apoptosis by mitochondrial dysfunction in rotenone-induced PC12 cells
Protocatechuic acid (PCA), a phenolic compound isolated from the kernels of Alpinia ( A.) oxyphylla, showed the significant neuroprotective effects on hydrogen peroxide (H 2O 2) or MPP +-induced apoptosis in cultured PC12 cells. However, the mechanism how PCA suppresses rotenone-induced neurotoxicit...
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| Veröffentlicht in: | Toxicology in vitro 2008-03, Vol.22 (2), p.430-437 |
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| creator | Liu, Ye-Ming Jiang, Bo Bao, Yong-Ming An, Li-Jia |
| description | Protocatechuic acid (PCA), a phenolic compound isolated from the kernels of
Alpinia (
A.)
oxyphylla, showed the significant neuroprotective effects on hydrogen peroxide (H
2O
2) or MPP
+-induced apoptosis in cultured PC12 cells. However, the mechanism how PCA suppresses rotenone-induced neurotoxicity in cultured PC12 cells remains unclear. In this study, we investigated the protective effects of PCA in PC12 cells exposed to rotenone as an in vitro model of mitochondrial dysfunction and apoptotic cell death. The apoptosis in rotenone-induced PC12 cells was accompanied by the loss of mitochondrial membrane potential, the formation of reactive oxygen species (ROS), the total glutathione depletion, activation of caspase-3 and down-regulation of Bcl-2. In contrast, PCA markedly attenuated the above-mentioned mitochondrial dysfunction in a dose-dependent manner. Taken together, these results suggest that treatment of PC12 cells with PCA can block rotenone-induced apoptosis via ameliorating the mitochondrial dysfunction. |
| doi_str_mv | 10.1016/j.tiv.2007.10.012 |
| format | Article |
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Alpinia (
A.)
oxyphylla, showed the significant neuroprotective effects on hydrogen peroxide (H
2O
2) or MPP
+-induced apoptosis in cultured PC12 cells. However, the mechanism how PCA suppresses rotenone-induced neurotoxicity in cultured PC12 cells remains unclear. In this study, we investigated the protective effects of PCA in PC12 cells exposed to rotenone as an in vitro model of mitochondrial dysfunction and apoptotic cell death. The apoptosis in rotenone-induced PC12 cells was accompanied by the loss of mitochondrial membrane potential, the formation of reactive oxygen species (ROS), the total glutathione depletion, activation of caspase-3 and down-regulation of Bcl-2. In contrast, PCA markedly attenuated the above-mentioned mitochondrial dysfunction in a dose-dependent manner. Taken together, these results suggest that treatment of PC12 cells with PCA can block rotenone-induced apoptosis via ameliorating the mitochondrial dysfunction.</description><identifier>ISSN: 0887-2333</identifier><identifier>EISSN: 1879-3177</identifier><identifier>DOI: 10.1016/j.tiv.2007.10.012</identifier><identifier>PMID: 18082360</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Alpinia ; Animals ; Anticarcinogenic Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Caspase 3 - metabolism ; Cell Nucleus - drug effects ; Cell Nucleus - ultrastructure ; Cell Survival - drug effects ; Dopamine - physiology ; Flow Cytometry ; Genes, bcl-2 - drug effects ; Genes, bcl-2 - genetics ; Glutathione - metabolism ; Hydroxybenzoates - pharmacology ; Membrane Potentials - drug effects ; Mitochondria - drug effects ; Mitochondrial dysfunction ; Necrosis ; Neurotoxicity Syndromes - pathology ; PC12 Cells ; Protocatechuic acid ; Rats ; Reactive Oxygen Species - metabolism ; Rotenone ; Rotenone - toxicity ; Uncoupling Agents - toxicity</subject><ispartof>Toxicology in vitro, 2008-03, Vol.22 (2), p.430-437</ispartof><rights>2007 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c382t-c696107aed5db6347149528a0fb98176062b73d160dffac27a51c5bdd4ea15f23</citedby><cites>FETCH-LOGICAL-c382t-c696107aed5db6347149528a0fb98176062b73d160dffac27a51c5bdd4ea15f23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.tiv.2007.10.012$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18082360$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Ye-Ming</creatorcontrib><creatorcontrib>Jiang, Bo</creatorcontrib><creatorcontrib>Bao, Yong-Ming</creatorcontrib><creatorcontrib>An, Li-Jia</creatorcontrib><title>Protocatechuic acid inhibits apoptosis by mitochondrial dysfunction in rotenone-induced PC12 cells</title><title>Toxicology in vitro</title><addtitle>Toxicol In Vitro</addtitle><description>Protocatechuic acid (PCA), a phenolic compound isolated from the kernels of
Alpinia (
A.)
oxyphylla, showed the significant neuroprotective effects on hydrogen peroxide (H
2O
2) or MPP
+-induced apoptosis in cultured PC12 cells. However, the mechanism how PCA suppresses rotenone-induced neurotoxicity in cultured PC12 cells remains unclear. In this study, we investigated the protective effects of PCA in PC12 cells exposed to rotenone as an in vitro model of mitochondrial dysfunction and apoptotic cell death. The apoptosis in rotenone-induced PC12 cells was accompanied by the loss of mitochondrial membrane potential, the formation of reactive oxygen species (ROS), the total glutathione depletion, activation of caspase-3 and down-regulation of Bcl-2. In contrast, PCA markedly attenuated the above-mentioned mitochondrial dysfunction in a dose-dependent manner. Taken together, these results suggest that treatment of PC12 cells with PCA can block rotenone-induced apoptosis via ameliorating the mitochondrial dysfunction.</description><subject>Alpinia</subject><subject>Animals</subject><subject>Anticarcinogenic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Nucleus - drug effects</subject><subject>Cell Nucleus - ultrastructure</subject><subject>Cell Survival - drug effects</subject><subject>Dopamine - physiology</subject><subject>Flow Cytometry</subject><subject>Genes, bcl-2 - drug effects</subject><subject>Genes, bcl-2 - genetics</subject><subject>Glutathione - metabolism</subject><subject>Hydroxybenzoates - pharmacology</subject><subject>Membrane Potentials - drug effects</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondrial dysfunction</subject><subject>Necrosis</subject><subject>Neurotoxicity Syndromes - pathology</subject><subject>PC12 Cells</subject><subject>Protocatechuic acid</subject><subject>Rats</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Rotenone</subject><subject>Rotenone - toxicity</subject><subject>Uncoupling Agents - toxicity</subject><issn>0887-2333</issn><issn>1879-3177</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFqGzEQhkVJaNwkD9BL0Sm3dUeSV5LJKZgkLQSaQ3oWWkmLx9iSI2kDfvvK2JBbT8MM3_zMfIR8ZzBnwOTPzbzix5wDqNbPgfEvZMa0WnaCKXVBZqC16rgQ4op8K2UDAL3m8JVcMQ2aCwkzMrzmVJOzNbj1hI5ah55iXOOAtVC7T_uaChY6HOgOG7hO0We0W-oPZZyiq5hi42lLCTHF0GH0kwuevq4Ypy5st-WGXI52W8LtuV6Tv0-Pb6tf3cuf59-rh5fOCc1r5-RSMlA2-N4PUiwUWyx7ri2Mw1IzJUHyQQnPJPhxtI4r2zPXD94vgmX9yMU1uTvl7nN6n0KpZofleIGNIU3FcJA9A64byE6gy6mUHEazz7iz-WAYmKNYszFNrDmKPY6a2Lbz4xw-DbvgPzfOJhtwfwJCe_EDQzbFYYhNBebgqvEJ_xP_D6VLikY</recordid><startdate>20080301</startdate><enddate>20080301</enddate><creator>Liu, Ye-Ming</creator><creator>Jiang, Bo</creator><creator>Bao, Yong-Ming</creator><creator>An, Li-Jia</creator><general>Elsevier Ltd</general><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>7TK</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20080301</creationdate><title>Protocatechuic acid inhibits apoptosis by mitochondrial dysfunction in rotenone-induced PC12 cells</title><author>Liu, Ye-Ming ; Jiang, Bo ; Bao, Yong-Ming ; An, Li-Jia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c382t-c696107aed5db6347149528a0fb98176062b73d160dffac27a51c5bdd4ea15f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Alpinia</topic><topic>Animals</topic><topic>Anticarcinogenic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Nucleus - drug effects</topic><topic>Cell Nucleus - ultrastructure</topic><topic>Cell Survival - drug effects</topic><topic>Dopamine - physiology</topic><topic>Flow Cytometry</topic><topic>Genes, bcl-2 - drug effects</topic><topic>Genes, bcl-2 - genetics</topic><topic>Glutathione - metabolism</topic><topic>Hydroxybenzoates - pharmacology</topic><topic>Membrane Potentials - drug effects</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondrial dysfunction</topic><topic>Necrosis</topic><topic>Neurotoxicity Syndromes - pathology</topic><topic>PC12 Cells</topic><topic>Protocatechuic acid</topic><topic>Rats</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Rotenone</topic><topic>Rotenone - toxicity</topic><topic>Uncoupling Agents - toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Ye-Ming</creatorcontrib><creatorcontrib>Jiang, Bo</creatorcontrib><creatorcontrib>Bao, Yong-Ming</creatorcontrib><creatorcontrib>An, Li-Jia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Toxicology in vitro</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Ye-Ming</au><au>Jiang, Bo</au><au>Bao, Yong-Ming</au><au>An, Li-Jia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protocatechuic acid inhibits apoptosis by mitochondrial dysfunction in rotenone-induced PC12 cells</atitle><jtitle>Toxicology in vitro</jtitle><addtitle>Toxicol In Vitro</addtitle><date>2008-03-01</date><risdate>2008</risdate><volume>22</volume><issue>2</issue><spage>430</spage><epage>437</epage><pages>430-437</pages><issn>0887-2333</issn><eissn>1879-3177</eissn><abstract>Protocatechuic acid (PCA), a phenolic compound isolated from the kernels of
Alpinia (
A.)
oxyphylla, showed the significant neuroprotective effects on hydrogen peroxide (H
2O
2) or MPP
+-induced apoptosis in cultured PC12 cells. However, the mechanism how PCA suppresses rotenone-induced neurotoxicity in cultured PC12 cells remains unclear. In this study, we investigated the protective effects of PCA in PC12 cells exposed to rotenone as an in vitro model of mitochondrial dysfunction and apoptotic cell death. The apoptosis in rotenone-induced PC12 cells was accompanied by the loss of mitochondrial membrane potential, the formation of reactive oxygen species (ROS), the total glutathione depletion, activation of caspase-3 and down-regulation of Bcl-2. In contrast, PCA markedly attenuated the above-mentioned mitochondrial dysfunction in a dose-dependent manner. Taken together, these results suggest that treatment of PC12 cells with PCA can block rotenone-induced apoptosis via ameliorating the mitochondrial dysfunction.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>18082360</pmid><doi>10.1016/j.tiv.2007.10.012</doi><tpages>8</tpages></addata></record> |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Alpinia Animals Anticarcinogenic Agents - pharmacology Apoptosis Apoptosis - drug effects Caspase 3 - metabolism Cell Nucleus - drug effects Cell Nucleus - ultrastructure Cell Survival - drug effects Dopamine - physiology Flow Cytometry Genes, bcl-2 - drug effects Genes, bcl-2 - genetics Glutathione - metabolism Hydroxybenzoates - pharmacology Membrane Potentials - drug effects Mitochondria - drug effects Mitochondrial dysfunction Necrosis Neurotoxicity Syndromes - pathology PC12 Cells Protocatechuic acid Rats Reactive Oxygen Species - metabolism Rotenone Rotenone - toxicity Uncoupling Agents - toxicity |
| title | Protocatechuic acid inhibits apoptosis by mitochondrial dysfunction in rotenone-induced PC12 cells |
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