Curcumin Attenuated Bupivacaine-Induced Neurotoxicity in SH-SY5Y Cells Via Activation of the Akt Signaling Pathway
Bupivacaine is widely used for regional anesthesia, spinal anesthesia, and pain management. However, bupivacaine could cause neuronal injury. Curcumin, a low molecular weight polyphenol, has a variety of bioactivities and may exert neuroprotective effects against damage induced by some stimuli. In t...
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| Veröffentlicht in: | Neurochemical research 2016-09, Vol.41 (9), p.2425-2432 |
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| creator | Fan, You-Ling Li, Heng-Chang Zhao, Wei Peng, Hui-Hua Huang, Fang Jiang, Wei-Hang Xu, Shi-Yuan |
| description | Bupivacaine is widely used for regional anesthesia, spinal anesthesia, and pain management. However, bupivacaine could cause neuronal injury. Curcumin, a low molecular weight polyphenol, has a variety of bioactivities and may exert neuroprotective effects against damage induced by some stimuli. In the present study, we tested whether curcumin could attenuate bupivacaine-induced neurotoxicity in SH-SY5Y cells. Cell injury was evaluated by examining cell viability, mitochondrial damage and apoptosis. We also investigated the levels of activation of the Akt signaling pathway and the effect of Akt inhibition by triciribine on cell injury following bupivacaine and curcumin treatment. Our findings showed that the bupivacaine treatment could induce neurotoxicity. Pretreatment of the SH-SY5Y cells with curcumin significantly attenuated bupivacaine-induced neurotoxicity. Interestingly, the curcumin treatment increased the levels of Akt phosphorylation. More significantly, the pharmacological inhibition of Akt abolished the cytoprotective effect of curcumin against bupivacaine-induced cell injury. Our data suggest that pretreating SH-SY5Y cells with curcumin provides a protective effect on bupivacaine-induced neuronal injury via activation of the Akt signaling pathway. |
| doi_str_mv | 10.1007/s11064-016-1955-4 |
| format | Article |
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However, bupivacaine could cause neuronal injury. Curcumin, a low molecular weight polyphenol, has a variety of bioactivities and may exert neuroprotective effects against damage induced by some stimuli. In the present study, we tested whether curcumin could attenuate bupivacaine-induced neurotoxicity in SH-SY5Y cells. Cell injury was evaluated by examining cell viability, mitochondrial damage and apoptosis. We also investigated the levels of activation of the Akt signaling pathway and the effect of Akt inhibition by triciribine on cell injury following bupivacaine and curcumin treatment. Our findings showed that the bupivacaine treatment could induce neurotoxicity. Pretreatment of the SH-SY5Y cells with curcumin significantly attenuated bupivacaine-induced neurotoxicity. Interestingly, the curcumin treatment increased the levels of Akt phosphorylation. More significantly, the pharmacological inhibition of Akt abolished the cytoprotective effect of curcumin against bupivacaine-induced cell injury. Our data suggest that pretreating SH-SY5Y cells with curcumin provides a protective effect on bupivacaine-induced neuronal injury via activation of the Akt signaling pathway.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-016-1955-4</identifier><identifier>PMID: 27233246</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Activation ; AKT protein ; Anesthesia ; Apoptosis ; Apoptosis - drug effects ; Attenuation ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Bupivacaine ; Bupivacaine - pharmacology ; Cell Biology ; Cell injury ; Cell Line, Tumor ; Cell Survival - drug effects ; Curcumin ; Curcumin - pharmacology ; Damage assessment ; Humans ; Inhibition ; Injuries ; Kinases ; Local anesthesia ; Low molecular weights ; Membrane Potential, Mitochondrial - drug effects ; Mitochondria ; Molecular weight ; Neurochemistry ; Neurology ; Neurons - drug effects ; Neurons - metabolism ; Neuroprotection ; Neuroprotective Agents - pharmacology ; Neurosciences ; Neurotoxicity ; Neurotoxicity Syndromes - drug therapy ; Neurotoxicity Syndromes - metabolism ; Original Paper ; Pain ; Pharmacology ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; Phosphorylation - drug effects ; Proto-Oncogene Proteins c-akt - metabolism ; Signal transduction ; Signal Transduction - drug effects ; Signaling</subject><ispartof>Neurochemical research, 2016-09, Vol.41 (9), p.2425-2432</ispartof><rights>Springer Science+Business Media New York 2016</rights><rights>Neurochemical Research is a copyright of Springer, (2016). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-2873a742037c2ad2808cb911c4e463707cb1c22b107e85541237a45f3536a0263</citedby><cites>FETCH-LOGICAL-c405t-2873a742037c2ad2808cb911c4e463707cb1c22b107e85541237a45f3536a0263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11064-016-1955-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11064-016-1955-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27233246$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fan, You-Ling</creatorcontrib><creatorcontrib>Li, Heng-Chang</creatorcontrib><creatorcontrib>Zhao, Wei</creatorcontrib><creatorcontrib>Peng, Hui-Hua</creatorcontrib><creatorcontrib>Huang, Fang</creatorcontrib><creatorcontrib>Jiang, Wei-Hang</creatorcontrib><creatorcontrib>Xu, Shi-Yuan</creatorcontrib><title>Curcumin Attenuated Bupivacaine-Induced Neurotoxicity in SH-SY5Y Cells Via Activation of the Akt Signaling Pathway</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>Bupivacaine is widely used for regional anesthesia, spinal anesthesia, and pain management. However, bupivacaine could cause neuronal injury. Curcumin, a low molecular weight polyphenol, has a variety of bioactivities and may exert neuroprotective effects against damage induced by some stimuli. In the present study, we tested whether curcumin could attenuate bupivacaine-induced neurotoxicity in SH-SY5Y cells. Cell injury was evaluated by examining cell viability, mitochondrial damage and apoptosis. We also investigated the levels of activation of the Akt signaling pathway and the effect of Akt inhibition by triciribine on cell injury following bupivacaine and curcumin treatment. Our findings showed that the bupivacaine treatment could induce neurotoxicity. Pretreatment of the SH-SY5Y cells with curcumin significantly attenuated bupivacaine-induced neurotoxicity. Interestingly, the curcumin treatment increased the levels of Akt phosphorylation. More significantly, the pharmacological inhibition of Akt abolished the cytoprotective effect of curcumin against bupivacaine-induced cell injury. Our data suggest that pretreating SH-SY5Y cells with curcumin provides a protective effect on bupivacaine-induced neuronal injury via activation of the Akt signaling pathway.</description><subject>Activation</subject><subject>AKT protein</subject><subject>Anesthesia</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Attenuation</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bupivacaine</subject><subject>Bupivacaine - pharmacology</subject><subject>Cell Biology</subject><subject>Cell injury</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Curcumin</subject><subject>Curcumin - pharmacology</subject><subject>Damage assessment</subject><subject>Humans</subject><subject>Inhibition</subject><subject>Injuries</subject><subject>Kinases</subject><subject>Local anesthesia</subject><subject>Low molecular weights</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mitochondria</subject><subject>Molecular weight</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neurosciences</subject><subject>Neurotoxicity</subject><subject>Neurotoxicity Syndromes - drug therapy</subject><subject>Neurotoxicity Syndromes - metabolism</subject><subject>Original Paper</subject><subject>Pain</subject><subject>Pharmacology</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kUtvUzEQha0KREPhB3RTWWLDxjDjx_XNMo2grVQBUgCpK8txnNRt4hv8gObf4yotlSqxGmnOd86MdAg5RviAAPpjRoROMsCO4VgpJg_ICJUWrBuDeEFGIJoqcAyH5HXONwDNxfEVOeSaC8FlNyJpWpOrmxDppBQfqy1-QU_rNvy2zobo2UVcVNd2X3xNQxnuggtlRxs_O2ezK3VFp369zvRnsHTiSrOVMEQ6LGm59nRyW-gsrKJdh7ii32y5_mN3b8jLpV1n__ZhHpEfnz99n56zy69nF9PJJXMSVGG818JqyUFox-2C99C7-RjRSS87oUG7OTrO5wja90pJ5EJbqZZCic4C78QReb_P3abhV_W5mE3Irn1rox9qNtgj9rrnKBr67hl6M9TU3s6myUqjgh4bhXvKpSHn5Jdmm8LGpp1BMPeFmH0hphVi7gsxsnlOHpLrfOMX_xyPDTSA74HcpLjy6en0_1P_Agwok2o</recordid><startdate>20160901</startdate><enddate>20160901</enddate><creator>Fan, You-Ling</creator><creator>Li, Heng-Chang</creator><creator>Zhao, Wei</creator><creator>Peng, Hui-Hua</creator><creator>Huang, Fang</creator><creator>Jiang, Wei-Hang</creator><creator>Xu, Shi-Yuan</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20160901</creationdate><title>Curcumin Attenuated Bupivacaine-Induced Neurotoxicity in SH-SY5Y Cells Via Activation of the Akt Signaling Pathway</title><author>Fan, You-Ling ; Li, Heng-Chang ; Zhao, Wei ; Peng, Hui-Hua ; Huang, Fang ; Jiang, Wei-Hang ; Xu, Shi-Yuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-2873a742037c2ad2808cb911c4e463707cb1c22b107e85541237a45f3536a0263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Activation</topic><topic>AKT protein</topic><topic>Anesthesia</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Attenuation</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bupivacaine</topic><topic>Bupivacaine - pharmacology</topic><topic>Cell Biology</topic><topic>Cell injury</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival - drug effects</topic><topic>Curcumin</topic><topic>Curcumin - pharmacology</topic><topic>Damage assessment</topic><topic>Humans</topic><topic>Inhibition</topic><topic>Injuries</topic><topic>Kinases</topic><topic>Local anesthesia</topic><topic>Low molecular weights</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mitochondria</topic><topic>Molecular weight</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neurosciences</topic><topic>Neurotoxicity</topic><topic>Neurotoxicity Syndromes - drug therapy</topic><topic>Neurotoxicity Syndromes - metabolism</topic><topic>Original Paper</topic><topic>Pain</topic><topic>Pharmacology</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fan, You-Ling</creatorcontrib><creatorcontrib>Li, Heng-Chang</creatorcontrib><creatorcontrib>Zhao, Wei</creatorcontrib><creatorcontrib>Peng, Hui-Hua</creatorcontrib><creatorcontrib>Huang, Fang</creatorcontrib><creatorcontrib>Jiang, Wei-Hang</creatorcontrib><creatorcontrib>Xu, Shi-Yuan</creatorcontrib><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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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</collection><collection>Environmental Sciences and Pollution Management</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>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>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><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fan, You-Ling</au><au>Li, Heng-Chang</au><au>Zhao, Wei</au><au>Peng, Hui-Hua</au><au>Huang, Fang</au><au>Jiang, Wei-Hang</au><au>Xu, Shi-Yuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Curcumin Attenuated Bupivacaine-Induced Neurotoxicity in SH-SY5Y Cells Via Activation of the Akt Signaling Pathway</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2016-09-01</date><risdate>2016</risdate><volume>41</volume><issue>9</issue><spage>2425</spage><epage>2432</epage><pages>2425-2432</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Bupivacaine is widely used for regional anesthesia, spinal anesthesia, and pain management. However, bupivacaine could cause neuronal injury. Curcumin, a low molecular weight polyphenol, has a variety of bioactivities and may exert neuroprotective effects against damage induced by some stimuli. In the present study, we tested whether curcumin could attenuate bupivacaine-induced neurotoxicity in SH-SY5Y cells. Cell injury was evaluated by examining cell viability, mitochondrial damage and apoptosis. We also investigated the levels of activation of the Akt signaling pathway and the effect of Akt inhibition by triciribine on cell injury following bupivacaine and curcumin treatment. Our findings showed that the bupivacaine treatment could induce neurotoxicity. Pretreatment of the SH-SY5Y cells with curcumin significantly attenuated bupivacaine-induced neurotoxicity. Interestingly, the curcumin treatment increased the levels of Akt phosphorylation. More significantly, the pharmacological inhibition of Akt abolished the cytoprotective effect of curcumin against bupivacaine-induced cell injury. Our data suggest that pretreating SH-SY5Y cells with curcumin provides a protective effect on bupivacaine-induced neuronal injury via activation of the Akt signaling pathway.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>27233246</pmid><doi>10.1007/s11064-016-1955-4</doi><tpages>8</tpages></addata></record> |
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| subjects | Activation AKT protein Anesthesia Apoptosis Apoptosis - drug effects Attenuation Biochemistry Biomedical and Life Sciences Biomedicine Bupivacaine Bupivacaine - pharmacology Cell Biology Cell injury Cell Line, Tumor Cell Survival - drug effects Curcumin Curcumin - pharmacology Damage assessment Humans Inhibition Injuries Kinases Local anesthesia Low molecular weights Membrane Potential, Mitochondrial - drug effects Mitochondria Molecular weight Neurochemistry Neurology Neurons - drug effects Neurons - metabolism Neuroprotection Neuroprotective Agents - pharmacology Neurosciences Neurotoxicity Neurotoxicity Syndromes - drug therapy Neurotoxicity Syndromes - metabolism Original Paper Pain Pharmacology Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Phosphorylation - drug effects Proto-Oncogene Proteins c-akt - metabolism Signal transduction Signal Transduction - drug effects Signaling |
| title | Curcumin Attenuated Bupivacaine-Induced Neurotoxicity in SH-SY5Y Cells Via Activation of the Akt Signaling Pathway |
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