Posttreatment with 11-Keto-β-Boswellic Acid Ameliorates Cerebral Ischemia–Reperfusion Injury: Nrf2/HO-1 Pathway as a Potential Mechanism
Oxidative stress is well known to play a pivotal role in cerebral ischemia–reperfusion injury. The nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway has been considered a potential target for neuroprotection in stroke. 11-Keto-β-boswellic acid (KBA) is a triterpenoid...
Gespeichert in:
| Veröffentlicht in: | Molecular neurobiology 2015-12, Vol.52 (3), p.1430-1439 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1439 |
|---|---|
| container_issue | 3 |
| container_start_page | 1430 |
| container_title | Molecular neurobiology |
| container_volume | 52 |
| creator | Ding, Yi Chen, MinChun Wang, MingMing Li, YuWen Wen, AiDong |
| description | Oxidative stress is well known to play a pivotal role in cerebral ischemia–reperfusion injury. The nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway has been considered a potential target for neuroprotection in stroke. 11-Keto-β-boswellic acid (KBA) is a triterpenoid compound from extracts of
Boswellia serrata
. The aim of the present study was to determine whether KBA, a novel Nrf2 activator, can protect against cerebral ischemic injury. Middle cerebral artery occlusion (MCAO) was operated on male Sprague–Dawley rats. KBA (25 mg/kg) applied 1 h after reperfusion significantly reduced infarct volumes and apoptotic cells as well as increased neurologic scores at 48 h after reperfusion. Meanwhile, posttreatment with KBA significantly decreased malondialdehyde (MDA) levels, restored the superoxide dismutase (SOD) activity, and increased the protein Nrf2 and HO-1 expression in brain tissues. In primary cultured astrocytes, KBA increased the Nrf2 and HO-1 expression, which provided protection against oxygen and glucose deprivation (OGD)-induced oxidative insult. But knockdown of Nrf2 or HO-1 attenuated the protective effect of KBA. In conclusion, these findings provide evidence that the neuroprotection of KBA against oxidative stress-induced ischemic injury involves the Nrf2/HO-1 pathway. |
| doi_str_mv | 10.1007/s12035-014-8929-9 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1722172555</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1722172555</sourcerecordid><originalsourceid>FETCH-LOGICAL-c447t-534a1264e73b29704184f2fa47a707aefa40a5be3389548781886fe79efdc1f03</originalsourceid><addsrcrecordid>eNqNkUFuEzEUhi0EoqFwADbISzamfh577GEXokIjCo0QrC1n8oY4yoyD7VGUHXuW3ISD9BA9CY5SWCJWtuTv_633PkKeA38FnOuLBIJXinGQzDSiYc0DMgGlGgZgxEMy4aapmK6lOSNPUtpwLgRw_ZicCSWVEEJPyI9FSDlHdLnHIdO9z2sKwN5jDuz2F3sT0h63W9_SaetXdNrj1ofoMiY6w4jL6LZ0nto19t7dff_5CXcYuzH5MND5sBnj4TX9GDtxcXXDgC5cXu_dgbpEHV2EXD70Jf8B27UbfOqfkked2yZ8dn-eky9vLz_Prtj1zbv5bHrNWil1ZqqSDkQtUVdL0WguwchOdE5qp7l2WG7cqSVWlWmUNNqAMXWHusFu1ULHq3Py8tS7i-HbiCnb3qe2jOkGDGOyoMuetFBK_QcKhuu65kcUTmgbQ0oRO7uLvnfxYIHboy570mWLLnvUZZuSeXFfPy57XP1N_PFTAHECUnkavmK0mzDGoWznH62_ATOwoSw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1718076605</pqid></control><display><type>article</type><title>Posttreatment with 11-Keto-β-Boswellic Acid Ameliorates Cerebral Ischemia–Reperfusion Injury: Nrf2/HO-1 Pathway as a Potential Mechanism</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Ding, Yi ; Chen, MinChun ; Wang, MingMing ; Li, YuWen ; Wen, AiDong</creator><creatorcontrib>Ding, Yi ; Chen, MinChun ; Wang, MingMing ; Li, YuWen ; Wen, AiDong</creatorcontrib><description>Oxidative stress is well known to play a pivotal role in cerebral ischemia–reperfusion injury. The nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway has been considered a potential target for neuroprotection in stroke. 11-Keto-β-boswellic acid (KBA) is a triterpenoid compound from extracts of
Boswellia serrata
. The aim of the present study was to determine whether KBA, a novel Nrf2 activator, can protect against cerebral ischemic injury. Middle cerebral artery occlusion (MCAO) was operated on male Sprague–Dawley rats. KBA (25 mg/kg) applied 1 h after reperfusion significantly reduced infarct volumes and apoptotic cells as well as increased neurologic scores at 48 h after reperfusion. Meanwhile, posttreatment with KBA significantly decreased malondialdehyde (MDA) levels, restored the superoxide dismutase (SOD) activity, and increased the protein Nrf2 and HO-1 expression in brain tissues. In primary cultured astrocytes, KBA increased the Nrf2 and HO-1 expression, which provided protection against oxygen and glucose deprivation (OGD)-induced oxidative insult. But knockdown of Nrf2 or HO-1 attenuated the protective effect of KBA. In conclusion, these findings provide evidence that the neuroprotection of KBA against oxidative stress-induced ischemic injury involves the Nrf2/HO-1 pathway.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-014-8929-9</identifier><identifier>PMID: 25452227</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Apoptosis - drug effects ; Astrocytes - drug effects ; Astrocytes - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Boswellia - chemistry ; Brain - pathology ; Brain Damage, Chronic - etiology ; Brain Damage, Chronic - prevention & control ; Cell Biology ; Cell Hypoxia ; Cells, Cultured ; Drug Evaluation, Preclinical ; Glucose - pharmacology ; Heme Oxygenase (Decyclizing) - biosynthesis ; Heme Oxygenase (Decyclizing) - genetics ; Heme Oxygenase (Decyclizing) - physiology ; Infarction, Middle Cerebral Artery - drug therapy ; Infarction, Middle Cerebral Artery - metabolism ; Infarction, Middle Cerebral Artery - pathology ; Male ; Malondialdehyde - analysis ; Nerve Tissue Proteins - biosynthesis ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - physiology ; Neurobiology ; Neurology ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - toxicity ; Neurosciences ; NF-E2-Related Factor 2 - biosynthesis ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - physiology ; Oxidative Stress - drug effects ; Phytotherapy ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - etiology ; Reperfusion Injury - metabolism ; Reperfusion Injury - prevention & control ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Superoxide Dismutase - metabolism ; Triterpenes - pharmacology ; Triterpenes - toxicity</subject><ispartof>Molecular neurobiology, 2015-12, Vol.52 (3), p.1430-1439</ispartof><rights>Springer Science+Business Media New York 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-534a1264e73b29704184f2fa47a707aefa40a5be3389548781886fe79efdc1f03</citedby><cites>FETCH-LOGICAL-c447t-534a1264e73b29704184f2fa47a707aefa40a5be3389548781886fe79efdc1f03</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/s12035-014-8929-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-014-8929-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25452227$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ding, Yi</creatorcontrib><creatorcontrib>Chen, MinChun</creatorcontrib><creatorcontrib>Wang, MingMing</creatorcontrib><creatorcontrib>Li, YuWen</creatorcontrib><creatorcontrib>Wen, AiDong</creatorcontrib><title>Posttreatment with 11-Keto-β-Boswellic Acid Ameliorates Cerebral Ischemia–Reperfusion Injury: Nrf2/HO-1 Pathway as a Potential Mechanism</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Oxidative stress is well known to play a pivotal role in cerebral ischemia–reperfusion injury. The nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway has been considered a potential target for neuroprotection in stroke. 11-Keto-β-boswellic acid (KBA) is a triterpenoid compound from extracts of
Boswellia serrata
. The aim of the present study was to determine whether KBA, a novel Nrf2 activator, can protect against cerebral ischemic injury. Middle cerebral artery occlusion (MCAO) was operated on male Sprague–Dawley rats. KBA (25 mg/kg) applied 1 h after reperfusion significantly reduced infarct volumes and apoptotic cells as well as increased neurologic scores at 48 h after reperfusion. Meanwhile, posttreatment with KBA significantly decreased malondialdehyde (MDA) levels, restored the superoxide dismutase (SOD) activity, and increased the protein Nrf2 and HO-1 expression in brain tissues. In primary cultured astrocytes, KBA increased the Nrf2 and HO-1 expression, which provided protection against oxygen and glucose deprivation (OGD)-induced oxidative insult. But knockdown of Nrf2 or HO-1 attenuated the protective effect of KBA. In conclusion, these findings provide evidence that the neuroprotection of KBA against oxidative stress-induced ischemic injury involves the Nrf2/HO-1 pathway.</description><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Apoptosis - drug effects</subject><subject>Astrocytes - drug effects</subject><subject>Astrocytes - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Boswellia - chemistry</subject><subject>Brain - pathology</subject><subject>Brain Damage, Chronic - etiology</subject><subject>Brain Damage, Chronic - prevention & control</subject><subject>Cell Biology</subject><subject>Cell Hypoxia</subject><subject>Cells, Cultured</subject><subject>Drug Evaluation, Preclinical</subject><subject>Glucose - pharmacology</subject><subject>Heme Oxygenase (Decyclizing) - biosynthesis</subject><subject>Heme Oxygenase (Decyclizing) - genetics</subject><subject>Heme Oxygenase (Decyclizing) - physiology</subject><subject>Infarction, Middle Cerebral Artery - drug therapy</subject><subject>Infarction, Middle Cerebral Artery - metabolism</subject><subject>Infarction, Middle Cerebral Artery - pathology</subject><subject>Male</subject><subject>Malondialdehyde - analysis</subject><subject>Nerve Tissue Proteins - biosynthesis</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - physiology</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - toxicity</subject><subject>Neurosciences</subject><subject>NF-E2-Related Factor 2 - biosynthesis</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - physiology</subject><subject>Oxidative Stress - drug effects</subject><subject>Phytotherapy</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - etiology</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Triterpenes - pharmacology</subject><subject>Triterpenes - toxicity</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUFuEzEUhi0EoqFwADbISzamfh577GEXokIjCo0QrC1n8oY4yoyD7VGUHXuW3ISD9BA9CY5SWCJWtuTv_633PkKeA38FnOuLBIJXinGQzDSiYc0DMgGlGgZgxEMy4aapmK6lOSNPUtpwLgRw_ZicCSWVEEJPyI9FSDlHdLnHIdO9z2sKwN5jDuz2F3sT0h63W9_SaetXdNrj1ofoMiY6w4jL6LZ0nto19t7dff_5CXcYuzH5MND5sBnj4TX9GDtxcXXDgC5cXu_dgbpEHV2EXD70Jf8B27UbfOqfkked2yZ8dn-eky9vLz_Prtj1zbv5bHrNWil1ZqqSDkQtUVdL0WguwchOdE5qp7l2WG7cqSVWlWmUNNqAMXWHusFu1ULHq3Py8tS7i-HbiCnb3qe2jOkGDGOyoMuetFBK_QcKhuu65kcUTmgbQ0oRO7uLvnfxYIHboy570mWLLnvUZZuSeXFfPy57XP1N_PFTAHECUnkavmK0mzDGoWznH62_ATOwoSw</recordid><startdate>20151201</startdate><enddate>20151201</enddate><creator>Ding, Yi</creator><creator>Chen, MinChun</creator><creator>Wang, MingMing</creator><creator>Li, YuWen</creator><creator>Wen, AiDong</creator><general>Springer US</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>7X8</scope><scope>7TK</scope></search><sort><creationdate>20151201</creationdate><title>Posttreatment with 11-Keto-β-Boswellic Acid Ameliorates Cerebral Ischemia–Reperfusion Injury: Nrf2/HO-1 Pathway as a Potential Mechanism</title><author>Ding, Yi ; Chen, MinChun ; Wang, MingMing ; Li, YuWen ; Wen, AiDong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-534a1264e73b29704184f2fa47a707aefa40a5be3389548781886fe79efdc1f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Antioxidants - therapeutic use</topic><topic>Apoptosis - drug effects</topic><topic>Astrocytes - drug effects</topic><topic>Astrocytes - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Boswellia - chemistry</topic><topic>Brain - pathology</topic><topic>Brain Damage, Chronic - etiology</topic><topic>Brain Damage, Chronic - prevention & control</topic><topic>Cell Biology</topic><topic>Cell Hypoxia</topic><topic>Cells, Cultured</topic><topic>Drug Evaluation, Preclinical</topic><topic>Glucose - pharmacology</topic><topic>Heme Oxygenase (Decyclizing) - biosynthesis</topic><topic>Heme Oxygenase (Decyclizing) - genetics</topic><topic>Heme Oxygenase (Decyclizing) - physiology</topic><topic>Infarction, Middle Cerebral Artery - drug therapy</topic><topic>Infarction, Middle Cerebral Artery - metabolism</topic><topic>Infarction, Middle Cerebral Artery - pathology</topic><topic>Male</topic><topic>Malondialdehyde - analysis</topic><topic>Nerve Tissue Proteins - biosynthesis</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - physiology</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - toxicity</topic><topic>Neurosciences</topic><topic>NF-E2-Related Factor 2 - biosynthesis</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>NF-E2-Related Factor 2 - physiology</topic><topic>Oxidative Stress - drug effects</topic><topic>Phytotherapy</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - etiology</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Triterpenes - pharmacology</topic><topic>Triterpenes - toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ding, Yi</creatorcontrib><creatorcontrib>Chen, MinChun</creatorcontrib><creatorcontrib>Wang, MingMing</creatorcontrib><creatorcontrib>Li, YuWen</creatorcontrib><creatorcontrib>Wen, AiDong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ding, Yi</au><au>Chen, MinChun</au><au>Wang, MingMing</au><au>Li, YuWen</au><au>Wen, AiDong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Posttreatment with 11-Keto-β-Boswellic Acid Ameliorates Cerebral Ischemia–Reperfusion Injury: Nrf2/HO-1 Pathway as a Potential Mechanism</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2015-12-01</date><risdate>2015</risdate><volume>52</volume><issue>3</issue><spage>1430</spage><epage>1439</epage><pages>1430-1439</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Oxidative stress is well known to play a pivotal role in cerebral ischemia–reperfusion injury. The nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway has been considered a potential target for neuroprotection in stroke. 11-Keto-β-boswellic acid (KBA) is a triterpenoid compound from extracts of
Boswellia serrata
. The aim of the present study was to determine whether KBA, a novel Nrf2 activator, can protect against cerebral ischemic injury. Middle cerebral artery occlusion (MCAO) was operated on male Sprague–Dawley rats. KBA (25 mg/kg) applied 1 h after reperfusion significantly reduced infarct volumes and apoptotic cells as well as increased neurologic scores at 48 h after reperfusion. Meanwhile, posttreatment with KBA significantly decreased malondialdehyde (MDA) levels, restored the superoxide dismutase (SOD) activity, and increased the protein Nrf2 and HO-1 expression in brain tissues. In primary cultured astrocytes, KBA increased the Nrf2 and HO-1 expression, which provided protection against oxygen and glucose deprivation (OGD)-induced oxidative insult. But knockdown of Nrf2 or HO-1 attenuated the protective effect of KBA. In conclusion, these findings provide evidence that the neuroprotection of KBA against oxidative stress-induced ischemic injury involves the Nrf2/HO-1 pathway.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>25452227</pmid><doi>10.1007/s12035-014-8929-9</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0893-7648 |
| ispartof | Molecular neurobiology, 2015-12, Vol.52 (3), p.1430-1439 |
| issn | 0893-7648 1559-1182 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1722172555 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Antioxidants - pharmacology Antioxidants - therapeutic use Apoptosis - drug effects Astrocytes - drug effects Astrocytes - metabolism Biomedical and Life Sciences Biomedicine Boswellia - chemistry Brain - pathology Brain Damage, Chronic - etiology Brain Damage, Chronic - prevention & control Cell Biology Cell Hypoxia Cells, Cultured Drug Evaluation, Preclinical Glucose - pharmacology Heme Oxygenase (Decyclizing) - biosynthesis Heme Oxygenase (Decyclizing) - genetics Heme Oxygenase (Decyclizing) - physiology Infarction, Middle Cerebral Artery - drug therapy Infarction, Middle Cerebral Artery - metabolism Infarction, Middle Cerebral Artery - pathology Male Malondialdehyde - analysis Nerve Tissue Proteins - biosynthesis Nerve Tissue Proteins - genetics Nerve Tissue Proteins - physiology Neurobiology Neurology Neuroprotective Agents - pharmacology Neuroprotective Agents - toxicity Neurosciences NF-E2-Related Factor 2 - biosynthesis NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - physiology Oxidative Stress - drug effects Phytotherapy Rats Rats, Sprague-Dawley Reperfusion Injury - etiology Reperfusion Injury - metabolism Reperfusion Injury - prevention & control Signal Transduction - drug effects Signal Transduction - physiology Superoxide Dismutase - metabolism Triterpenes - pharmacology Triterpenes - toxicity |
| title | Posttreatment with 11-Keto-β-Boswellic Acid Ameliorates Cerebral Ischemia–Reperfusion Injury: Nrf2/HO-1 Pathway as a Potential Mechanism |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-31T17%3A49%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Posttreatment%20with%2011-Keto-%CE%B2-Boswellic%20Acid%20Ameliorates%20Cerebral%20Ischemia%E2%80%93Reperfusion%20Injury:%20Nrf2/HO-1%20Pathway%20as%20a%20Potential%20Mechanism&rft.jtitle=Molecular%20neurobiology&rft.au=Ding,%20Yi&rft.date=2015-12-01&rft.volume=52&rft.issue=3&rft.spage=1430&rft.epage=1439&rft.pages=1430-1439&rft.issn=0893-7648&rft.eissn=1559-1182&rft_id=info:doi/10.1007/s12035-014-8929-9&rft_dat=%3Cproquest_cross%3E1722172555%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1718076605&rft_id=info:pmid/25452227&rfr_iscdi=true |