The neuroprotective action of pyrroloquinoline quinone against glutamate-induced apoptosis in hippocampal neurons is mediated through the activation of PI3K/Akt pathway
Pyrroloquinoline quinone (PQQ), a cofactor in several enzyme-catalyzed redox reactions, possesses a potential capability of scavenging reactive oxygen species (ROS) and inhibiting cell apoptosis. In this study, we investigated the effects of PQQ on glutamate-induced cell death in primary cultured hi...
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| Veröffentlicht in: | Toxicology and applied pharmacology 2011-04, Vol.252 (1), p.62-72 |
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| creator | Zhang, Qi Shen, Mi Ding, Mei Shen, Dingding Ding, Fei |
| description | Pyrroloquinoline quinone (PQQ), a cofactor in several enzyme-catalyzed redox reactions, possesses a potential capability of scavenging reactive oxygen species (ROS) and inhibiting cell apoptosis. In this study, we investigated the effects of PQQ on glutamate-induced cell death in primary cultured hippocampal neurons and the possible underlying mechanisms. We found that glutamate-induced apoptosis in cultured hippocampal neurons was significantly attenuated by the ensuing PQQ treatment, which also inhibited the glutamate-induced increase in Ca2+ influx, caspase-3 activity, and ROS production, and reversed the glutamate-induced decrease in Bcl-2/Bax ratio. The examination of signaling pathways revealed that PQQ treatment activated the phosphorylation of Akt and suppressed the glutamate-induced phosphorylation of c-Jun N-terminal protein kinase (JNK). And inhibition of phosphatidylinositol-3-kinase (PI3K)/Akt cascade by LY294002 and wortmannin significantly blocked the protective effects of PQQ, and alleviated the increase in Bcl-2/Bax ratio. Taken together, our results indicated that PQQ could protect primary cultured hippocampal neurons against glutamate-induced cell damage by scavenging ROS, reducing Ca2+ influx, and caspase-3 activity, and suggested that PQQ-activated PI3K/Akt signaling might be responsible for its neuroprotective action through modulation of glutamate-induced imbalance between Bcl-2 and Bax.
►PQQ attenuated glutamate-induced cell apoptosis of cultured hippocampal neurons. ►PQQ inhibited glutamate-induced Ca2+ influx and caspase-3 activity. ►PQQ reduced glutamate-induced increase in ROS production. ►PQQ affected phosphorylation of Akt and JNK signalings after glutamate injury. ►PI3K/Akt was required for neuroprotection of PQQ by modulating Bcl-2/Bax ratio. |
| doi_str_mv | 10.1016/j.taap.2011.02.006 |
| format | Article |
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►PQQ attenuated glutamate-induced cell apoptosis of cultured hippocampal neurons. ►PQQ inhibited glutamate-induced Ca2+ influx and caspase-3 activity. ►PQQ reduced glutamate-induced increase in ROS production. ►PQQ affected phosphorylation of Akt and JNK signalings after glutamate injury. ►PI3K/Akt was required for neuroprotection of PQQ by modulating Bcl-2/Bax ratio.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1016/j.taap.2011.02.006</identifier><identifier>PMID: 21320517</identifier><identifier>CODEN: TXAPA9</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; Akt signaling ; ANIMAL CELLS ; Animals ; APOPTOSIS ; Apoptosis - drug effects ; Apoptosis - physiology ; AROMATICS ; BENZOQUINONES ; Biological and medical sciences ; CALCIUM IONS ; Cell Survival - drug effects ; Cell Survival - physiology ; Cells, Cultured ; CHARGED PARTICLES ; CHEMICAL REACTIONS ; Enzyme Activation - drug effects ; Enzyme Activation - physiology ; ENZYMES ; Female ; Glutamate ; Glutamic Acid - toxicity ; Hippocampal neurons ; Hippocampus - drug effects ; Hippocampus - metabolism ; INHIBITION ; IONS ; Medical sciences ; NERVE CELLS ; Neurons - drug effects ; Neurons - metabolism ; Neuroprotective Agents - pharmacology ; ORGANIC COMPOUNDS ; ORGANIC OXYGEN COMPOUNDS ; OXIDOREDUCTASES ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphatidylinositol 3-Kinases - physiology ; PHOSPHORYLATION ; PQQ Cofactor - pharmacology ; Pregnancy ; PROTEINS ; Proto-Oncogene Proteins c-akt - metabolism ; Proto-Oncogene Proteins c-akt - physiology ; Pyrroloquinoline quinone ; QUINONES ; Rats ; Rats, Sprague-Dawley ; Reactive oxygen species ; REDOX REACTIONS ; SCAVENGING ; Signal Transduction - drug effects ; Signal Transduction - physiology ; SOMATIC CELLS ; SUPEROXIDE DISMUTASE ; Toxicology ; TRANSCRIPTION FACTORS</subject><ispartof>Toxicology and applied pharmacology, 2011-04, Vol.252 (1), p.62-72</ispartof><rights>2011 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-6d3afc9166945fea30c73bf419283086067d552c00d4ccbbd9ed1bbd585f24c63</citedby><cites>FETCH-LOGICAL-c511t-6d3afc9166945fea30c73bf419283086067d552c00d4ccbbd9ed1bbd585f24c63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0041008X11000524$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24073634$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21320517$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/21535263$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Qi</creatorcontrib><creatorcontrib>Shen, Mi</creatorcontrib><creatorcontrib>Ding, Mei</creatorcontrib><creatorcontrib>Shen, Dingding</creatorcontrib><creatorcontrib>Ding, Fei</creatorcontrib><title>The neuroprotective action of pyrroloquinoline quinone against glutamate-induced apoptosis in hippocampal neurons is mediated through the activation of PI3K/Akt pathway</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>Pyrroloquinoline quinone (PQQ), a cofactor in several enzyme-catalyzed redox reactions, possesses a potential capability of scavenging reactive oxygen species (ROS) and inhibiting cell apoptosis. In this study, we investigated the effects of PQQ on glutamate-induced cell death in primary cultured hippocampal neurons and the possible underlying mechanisms. We found that glutamate-induced apoptosis in cultured hippocampal neurons was significantly attenuated by the ensuing PQQ treatment, which also inhibited the glutamate-induced increase in Ca2+ influx, caspase-3 activity, and ROS production, and reversed the glutamate-induced decrease in Bcl-2/Bax ratio. The examination of signaling pathways revealed that PQQ treatment activated the phosphorylation of Akt and suppressed the glutamate-induced phosphorylation of c-Jun N-terminal protein kinase (JNK). And inhibition of phosphatidylinositol-3-kinase (PI3K)/Akt cascade by LY294002 and wortmannin significantly blocked the protective effects of PQQ, and alleviated the increase in Bcl-2/Bax ratio. Taken together, our results indicated that PQQ could protect primary cultured hippocampal neurons against glutamate-induced cell damage by scavenging ROS, reducing Ca2+ influx, and caspase-3 activity, and suggested that PQQ-activated PI3K/Akt signaling might be responsible for its neuroprotective action through modulation of glutamate-induced imbalance between Bcl-2 and Bax.
►PQQ attenuated glutamate-induced cell apoptosis of cultured hippocampal neurons. ►PQQ inhibited glutamate-induced Ca2+ influx and caspase-3 activity. ►PQQ reduced glutamate-induced increase in ROS production. ►PQQ affected phosphorylation of Akt and JNK signalings after glutamate injury. ►PI3K/Akt was required for neuroprotection of PQQ by modulating Bcl-2/Bax ratio.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>Akt signaling</subject><subject>ANIMAL CELLS</subject><subject>Animals</subject><subject>APOPTOSIS</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>AROMATICS</subject><subject>BENZOQUINONES</subject><subject>Biological and medical sciences</subject><subject>CALCIUM IONS</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - physiology</subject><subject>Cells, Cultured</subject><subject>CHARGED PARTICLES</subject><subject>CHEMICAL REACTIONS</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme Activation - physiology</subject><subject>ENZYMES</subject><subject>Female</subject><subject>Glutamate</subject><subject>Glutamic Acid - toxicity</subject><subject>Hippocampal neurons</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>INHIBITION</subject><subject>IONS</subject><subject>Medical sciences</subject><subject>NERVE CELLS</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>ORGANIC COMPOUNDS</subject><subject>ORGANIC OXYGEN COMPOUNDS</subject><subject>OXIDOREDUCTASES</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - physiology</subject><subject>PHOSPHORYLATION</subject><subject>PQQ Cofactor - pharmacology</subject><subject>Pregnancy</subject><subject>PROTEINS</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - physiology</subject><subject>Pyrroloquinoline quinone</subject><subject>QUINONES</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive oxygen species</subject><subject>REDOX REACTIONS</subject><subject>SCAVENGING</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>SOMATIC CELLS</subject><subject>SUPEROXIDE DISMUTASE</subject><subject>Toxicology</subject><subject>TRANSCRIPTION FACTORS</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kctuEzEUhkcIREvhBVggSwixmvT4mozEpqq4VFSCRZHYWSceT8ZhYk9tT1DeiMfEYVLYsfot6zu3_6-qlxQWFKi63C4y4rhgQOkC2AJAParOKTSqBs754-ocQNAaYPX9rHqW0hYAGiHo0-qMUc5A0uV59euut8TbKYYxhmxNdntLsEjwJHRkPMQYhnA_OR8G5y358yqKG3Q-ZbIZpow7zLZ2vp2MbQmOYcwhuUScJ70bx2BwN-IwT_HlO5GdbV2paUnuY5g2fdF56h4fJn-94Z8vr35kMmLuf-LhefWkwyHZFye9qL59eH93_am-_fLx5vrqtjaS0lyrlmNnGqpUI2RnkYNZ8nUnaMNWHFYK1LKVkhmAVhizXreNbWkRuZIdE0bxi-r13Dek7HQyrpjSm-B98UYzKrlkihfq7UwV1-4nm7LeuWTsMKC3YUq6kUJJwdmykGwmTQwpRdvpMbodxoOmoI8x6q0-xqiPMWpgusRYil6d2k_r4tXfkofcCvDmBGAyOHQRvXHpHydgyRUXhXs3c7ZYtnc2Hi-yvuTk4vGgNrj_7fEbLgS_YA</recordid><startdate>20110401</startdate><enddate>20110401</enddate><creator>Zhang, Qi</creator><creator>Shen, Mi</creator><creator>Ding, Mei</creator><creator>Shen, Dingding</creator><creator>Ding, Fei</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</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>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>OTOTI</scope></search><sort><creationdate>20110401</creationdate><title>The neuroprotective action of pyrroloquinoline quinone against glutamate-induced apoptosis in hippocampal neurons is mediated through the activation of PI3K/Akt pathway</title><author>Zhang, Qi ; Shen, Mi ; Ding, Mei ; Shen, Dingding ; Ding, Fei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-6d3afc9166945fea30c73bf419283086067d552c00d4ccbbd9ed1bbd585f24c63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>Akt signaling</topic><topic>ANIMAL CELLS</topic><topic>Animals</topic><topic>APOPTOSIS</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>AROMATICS</topic><topic>BENZOQUINONES</topic><topic>Biological and medical sciences</topic><topic>CALCIUM IONS</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - physiology</topic><topic>Cells, Cultured</topic><topic>CHARGED PARTICLES</topic><topic>CHEMICAL REACTIONS</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzyme Activation - physiology</topic><topic>ENZYMES</topic><topic>Female</topic><topic>Glutamate</topic><topic>Glutamic Acid - toxicity</topic><topic>Hippocampal neurons</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>INHIBITION</topic><topic>IONS</topic><topic>Medical sciences</topic><topic>NERVE CELLS</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>ORGANIC COMPOUNDS</topic><topic>ORGANIC OXYGEN COMPOUNDS</topic><topic>OXIDOREDUCTASES</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - physiology</topic><topic>PHOSPHORYLATION</topic><topic>PQQ Cofactor - pharmacology</topic><topic>Pregnancy</topic><topic>PROTEINS</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - physiology</topic><topic>Pyrroloquinoline quinone</topic><topic>QUINONES</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive oxygen species</topic><topic>REDOX REACTIONS</topic><topic>SCAVENGING</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>SOMATIC CELLS</topic><topic>SUPEROXIDE DISMUTASE</topic><topic>Toxicology</topic><topic>TRANSCRIPTION FACTORS</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Qi</creatorcontrib><creatorcontrib>Shen, Mi</creatorcontrib><creatorcontrib>Ding, Mei</creatorcontrib><creatorcontrib>Shen, Dingding</creatorcontrib><creatorcontrib>Ding, Fei</creatorcontrib><collection>Pascal-Francis</collection><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><collection>OSTI.GOV</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Qi</au><au>Shen, Mi</au><au>Ding, Mei</au><au>Shen, Dingding</au><au>Ding, Fei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The neuroprotective action of pyrroloquinoline quinone against glutamate-induced apoptosis in hippocampal neurons is mediated through the activation of PI3K/Akt pathway</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2011-04-01</date><risdate>2011</risdate><volume>252</volume><issue>1</issue><spage>62</spage><epage>72</epage><pages>62-72</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>Pyrroloquinoline quinone (PQQ), a cofactor in several enzyme-catalyzed redox reactions, possesses a potential capability of scavenging reactive oxygen species (ROS) and inhibiting cell apoptosis. In this study, we investigated the effects of PQQ on glutamate-induced cell death in primary cultured hippocampal neurons and the possible underlying mechanisms. We found that glutamate-induced apoptosis in cultured hippocampal neurons was significantly attenuated by the ensuing PQQ treatment, which also inhibited the glutamate-induced increase in Ca2+ influx, caspase-3 activity, and ROS production, and reversed the glutamate-induced decrease in Bcl-2/Bax ratio. The examination of signaling pathways revealed that PQQ treatment activated the phosphorylation of Akt and suppressed the glutamate-induced phosphorylation of c-Jun N-terminal protein kinase (JNK). And inhibition of phosphatidylinositol-3-kinase (PI3K)/Akt cascade by LY294002 and wortmannin significantly blocked the protective effects of PQQ, and alleviated the increase in Bcl-2/Bax ratio. Taken together, our results indicated that PQQ could protect primary cultured hippocampal neurons against glutamate-induced cell damage by scavenging ROS, reducing Ca2+ influx, and caspase-3 activity, and suggested that PQQ-activated PI3K/Akt signaling might be responsible for its neuroprotective action through modulation of glutamate-induced imbalance between Bcl-2 and Bax.
►PQQ attenuated glutamate-induced cell apoptosis of cultured hippocampal neurons. ►PQQ inhibited glutamate-induced Ca2+ influx and caspase-3 activity. ►PQQ reduced glutamate-induced increase in ROS production. ►PQQ affected phosphorylation of Akt and JNK signalings after glutamate injury. ►PI3K/Akt was required for neuroprotection of PQQ by modulating Bcl-2/Bax ratio.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>21320517</pmid><doi>10.1016/j.taap.2011.02.006</doi><tpages>11</tpages></addata></record> |
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| ispartof | Toxicology and applied pharmacology, 2011-04, Vol.252 (1), p.62-72 |
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| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | 60 APPLIED LIFE SCIENCES Akt signaling ANIMAL CELLS Animals APOPTOSIS Apoptosis - drug effects Apoptosis - physiology AROMATICS BENZOQUINONES Biological and medical sciences CALCIUM IONS Cell Survival - drug effects Cell Survival - physiology Cells, Cultured CHARGED PARTICLES CHEMICAL REACTIONS Enzyme Activation - drug effects Enzyme Activation - physiology ENZYMES Female Glutamate Glutamic Acid - toxicity Hippocampal neurons Hippocampus - drug effects Hippocampus - metabolism INHIBITION IONS Medical sciences NERVE CELLS Neurons - drug effects Neurons - metabolism Neuroprotective Agents - pharmacology ORGANIC COMPOUNDS ORGANIC OXYGEN COMPOUNDS OXIDOREDUCTASES Phosphatidylinositol 3-Kinases - metabolism Phosphatidylinositol 3-Kinases - physiology PHOSPHORYLATION PQQ Cofactor - pharmacology Pregnancy PROTEINS Proto-Oncogene Proteins c-akt - metabolism Proto-Oncogene Proteins c-akt - physiology Pyrroloquinoline quinone QUINONES Rats Rats, Sprague-Dawley Reactive oxygen species REDOX REACTIONS SCAVENGING Signal Transduction - drug effects Signal Transduction - physiology SOMATIC CELLS SUPEROXIDE DISMUTASE Toxicology TRANSCRIPTION FACTORS |
| title | The neuroprotective action of pyrroloquinoline quinone against glutamate-induced apoptosis in hippocampal neurons is mediated through the activation of PI3K/Akt pathway |
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