Osthole Reverses Beta-Amyloid Peptide Cytotoxicity on Neural Cells by Enhancing Cyclic AMP Response Element-Binding Protein Phosphorylation
Accumulation of β-amyloid peptide (Aβ) in the brain plays an important role in the pathogenesis of Alzheimer’s disease (AD). Previous studies have demonstrated the neuroprotective role of osthole against oxygen and glucose deprivation in cortical neurons. However, the effects of osthole on Aβ-induce...
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| Veröffentlicht in: | Biological & pharmaceutical bulletin 2013/12/01, Vol.36(12), pp.1950-1958 |
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| creator | Hu, Yu Wen, Qingping Liang, Wenbo Kang, Tingguo Ren, Lu Zhang, Nan Zhao, Dan Sun, Dong Yang, Jingxian |
| description | Accumulation of β-amyloid peptide (Aβ) in the brain plays an important role in the pathogenesis of Alzheimer’s disease (AD). Previous studies have demonstrated the neuroprotective role of osthole against oxygen and glucose deprivation in cortical neurons. However, the effects of osthole on Aβ-induced neurotoxicity in neural cells have rarely been reported. The current study was designed to investigate the protective effects of osthole on a cell model of AD insulted by exogenous Aβ25-35 and the potential mechanism(s). In this study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, immunofluorescence analysis, apoptosis assay, reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) techniques were used in primary cortical neurons and SH-SY5Y cells. Our data showed that osthole reduced intracellular Aβ levels in neural cells, which was associated with decreased BACE1 protein; osthole reversed exogenous Aβ25-35-induced cell viability loss, apoptosis, and synapsin-1 reduction, which was related to the reestablishment of phosphorylation of cyclic AMP response element-binding protein (CREB). The collective evidence indicates that osthole possesses the ability to protect cortical neurons and SH-SY5Y cells against Aβ injury, and the underlying mechanism may be attributed to the enhancement of CREB phosphorylation. |
| doi_str_mv | 10.1248/bpb.b13-00561 |
| format | Article |
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Previous studies have demonstrated the neuroprotective role of osthole against oxygen and glucose deprivation in cortical neurons. However, the effects of osthole on Aβ-induced neurotoxicity in neural cells have rarely been reported. The current study was designed to investigate the protective effects of osthole on a cell model of AD insulted by exogenous Aβ25-35 and the potential mechanism(s). In this study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, immunofluorescence analysis, apoptosis assay, reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) techniques were used in primary cortical neurons and SH-SY5Y cells. Our data showed that osthole reduced intracellular Aβ levels in neural cells, which was associated with decreased BACE1 protein; osthole reversed exogenous Aβ25-35-induced cell viability loss, apoptosis, and synapsin-1 reduction, which was related to the reestablishment of phosphorylation of cyclic AMP response element-binding protein (CREB). The collective evidence indicates that osthole possesses the ability to protect cortical neurons and SH-SY5Y cells against Aβ injury, and the underlying mechanism may be attributed to the enhancement of CREB phosphorylation.</description><identifier>ISSN: 0918-6158</identifier><identifier>EISSN: 1347-5215</identifier><identifier>DOI: 10.1248/bpb.b13-00561</identifier><identifier>PMID: 24432380</identifier><language>eng</language><publisher>Japan: The Pharmaceutical Society of Japan</publisher><subject>Alzheimer’s disease ; Amyloid beta-Peptides - toxicity ; Amyloid Precursor Protein Secretases - metabolism ; Animals ; Aspartic Acid Endopeptidases - metabolism ; bcl-2-Associated X Protein - genetics ; Cell Line, Tumor ; Cells, Cultured ; Coumarins - pharmacology ; cyclic AMP response element-binding protein ; Cyclic AMP Response Element-Binding Protein - genetics ; Cyclic AMP Response Element-Binding Protein - metabolism ; Humans ; Mice ; Mice, Inbred C57BL ; Neurons - drug effects ; Neurons - metabolism ; Neuroprotective Agents - pharmacology ; osthole ; Peptide Fragments - toxicity ; Phosphorylation - drug effects ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Synapsins - metabolism ; β-amyloid peptide25-35</subject><ispartof>Biological and Pharmaceutical Bulletin, 2013/12/01, Vol.36(12), pp.1950-1958</ispartof><rights>2013 The Pharmaceutical Society of Japan</rights><rights>Copyright Japan Science and Technology Agency 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c568t-4e7df21b81545a9b77ead97078fa4fd4f66fb27436a043da88d458766c64ac483</citedby><cites>FETCH-LOGICAL-c568t-4e7df21b81545a9b77ead97078fa4fd4f66fb27436a043da88d458766c64ac483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,1885,27931,27932</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24432380$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Yu</creatorcontrib><creatorcontrib>Wen, Qingping</creatorcontrib><creatorcontrib>Liang, Wenbo</creatorcontrib><creatorcontrib>Kang, Tingguo</creatorcontrib><creatorcontrib>Ren, Lu</creatorcontrib><creatorcontrib>Zhang, Nan</creatorcontrib><creatorcontrib>Zhao, Dan</creatorcontrib><creatorcontrib>Sun, Dong</creatorcontrib><creatorcontrib>Yang, Jingxian</creatorcontrib><title>Osthole Reverses Beta-Amyloid Peptide Cytotoxicity on Neural Cells by Enhancing Cyclic AMP Response Element-Binding Protein Phosphorylation</title><title>Biological & pharmaceutical bulletin</title><addtitle>Biol Pharm Bull</addtitle><description>Accumulation of β-amyloid peptide (Aβ) in the brain plays an important role in the pathogenesis of Alzheimer’s disease (AD). Previous studies have demonstrated the neuroprotective role of osthole against oxygen and glucose deprivation in cortical neurons. However, the effects of osthole on Aβ-induced neurotoxicity in neural cells have rarely been reported. The current study was designed to investigate the protective effects of osthole on a cell model of AD insulted by exogenous Aβ25-35 and the potential mechanism(s). In this study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, immunofluorescence analysis, apoptosis assay, reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) techniques were used in primary cortical neurons and SH-SY5Y cells. Our data showed that osthole reduced intracellular Aβ levels in neural cells, which was associated with decreased BACE1 protein; osthole reversed exogenous Aβ25-35-induced cell viability loss, apoptosis, and synapsin-1 reduction, which was related to the reestablishment of phosphorylation of cyclic AMP response element-binding protein (CREB). The collective evidence indicates that osthole possesses the ability to protect cortical neurons and SH-SY5Y cells against Aβ injury, and the underlying mechanism may be attributed to the enhancement of CREB phosphorylation.</description><subject>Alzheimer’s disease</subject><subject>Amyloid beta-Peptides - toxicity</subject><subject>Amyloid Precursor Protein Secretases - metabolism</subject><subject>Animals</subject><subject>Aspartic Acid Endopeptidases - metabolism</subject><subject>bcl-2-Associated X Protein - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cells, Cultured</subject><subject>Coumarins - pharmacology</subject><subject>cyclic AMP response element-binding protein</subject><subject>Cyclic AMP Response Element-Binding Protein - genetics</subject><subject>Cyclic AMP Response Element-Binding Protein - metabolism</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>osthole</subject><subject>Peptide Fragments - toxicity</subject><subject>Phosphorylation - drug effects</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Synapsins - metabolism</subject><subject>β-amyloid peptide25-35</subject><issn>0918-6158</issn><issn>1347-5215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0U-P1CAcxvHGaNxx9ejVkHjx0hUKBeY4Ozv-SVZ3YvTcUPrrlgmFCtTY1-CbltlZ5-ClHPrJN5CnKF4TfEUqJt-3U3vVElpiXHPypFgRykRZV6R-WqzwmsiSk1peFC9iPGCMBa7o8-KiYoxWVOJV8ecupsFbQN_gF4QIEV1DUuVmXKw3HdrDlEwHaLskn_xvo01akHfoK8xBWbQFayNqF7Rzg3LauPsstTUabb7sczJO3kVAOwsjuFReG9cdzT74BMah_eDjNPiwWJWMdy-LZ72yEV49npfFjw-779tP5e3dx8_bzW2pay5TyUB0fUVaSWpWq3UrBKhuLbCQvWJ9x3rO-7YSjHKFGe2UlB2rpeBcc6Y0k_SyeHfqTsH_nCGmZjRR56coB36ODWFrzNeM1jjTt__Rg5-Dy7fLSkgsBeN1VuVJ6eBjDNA3UzCjCktDcHNcqckrNXml5mGl7N88Vud2hO6s_82Swc0JHGJS93AGKiSjLTzkKM_p4_fcPf_WgwoNOPoXRbCm3Q</recordid><startdate>20131201</startdate><enddate>20131201</enddate><creator>Hu, Yu</creator><creator>Wen, Qingping</creator><creator>Liang, Wenbo</creator><creator>Kang, Tingguo</creator><creator>Ren, Lu</creator><creator>Zhang, Nan</creator><creator>Zhao, Dan</creator><creator>Sun, Dong</creator><creator>Yang, Jingxian</creator><general>The Pharmaceutical Society of Japan</general><general>Japan Science and Technology Agency</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20131201</creationdate><title>Osthole Reverses Beta-Amyloid Peptide Cytotoxicity on Neural Cells by Enhancing Cyclic AMP Response Element-Binding Protein Phosphorylation</title><author>Hu, Yu ; Wen, Qingping ; Liang, Wenbo ; Kang, Tingguo ; Ren, Lu ; Zhang, Nan ; Zhao, Dan ; Sun, Dong ; Yang, Jingxian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c568t-4e7df21b81545a9b77ead97078fa4fd4f66fb27436a043da88d458766c64ac483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Alzheimer’s disease</topic><topic>Amyloid beta-Peptides - toxicity</topic><topic>Amyloid Precursor Protein Secretases - metabolism</topic><topic>Animals</topic><topic>Aspartic Acid Endopeptidases - metabolism</topic><topic>bcl-2-Associated X Protein - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cells, Cultured</topic><topic>Coumarins - pharmacology</topic><topic>cyclic AMP response element-binding protein</topic><topic>Cyclic AMP Response Element-Binding Protein - genetics</topic><topic>Cyclic AMP Response Element-Binding Protein - metabolism</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>osthole</topic><topic>Peptide Fragments - toxicity</topic><topic>Phosphorylation - drug effects</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Synapsins - metabolism</topic><topic>β-amyloid peptide25-35</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Yu</creatorcontrib><creatorcontrib>Wen, Qingping</creatorcontrib><creatorcontrib>Liang, Wenbo</creatorcontrib><creatorcontrib>Kang, Tingguo</creatorcontrib><creatorcontrib>Ren, Lu</creatorcontrib><creatorcontrib>Zhang, Nan</creatorcontrib><creatorcontrib>Zhao, Dan</creatorcontrib><creatorcontrib>Sun, Dong</creatorcontrib><creatorcontrib>Yang, Jingxian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biological & pharmaceutical bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Yu</au><au>Wen, Qingping</au><au>Liang, Wenbo</au><au>Kang, Tingguo</au><au>Ren, Lu</au><au>Zhang, Nan</au><au>Zhao, Dan</au><au>Sun, Dong</au><au>Yang, Jingxian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Osthole Reverses Beta-Amyloid Peptide Cytotoxicity on Neural Cells by Enhancing Cyclic AMP Response Element-Binding Protein Phosphorylation</atitle><jtitle>Biological & pharmaceutical bulletin</jtitle><addtitle>Biol Pharm Bull</addtitle><date>2013-12-01</date><risdate>2013</risdate><volume>36</volume><issue>12</issue><spage>1950</spage><epage>1958</epage><pages>1950-1958</pages><issn>0918-6158</issn><eissn>1347-5215</eissn><abstract>Accumulation of β-amyloid peptide (Aβ) in the brain plays an important role in the pathogenesis of Alzheimer’s disease (AD). Previous studies have demonstrated the neuroprotective role of osthole against oxygen and glucose deprivation in cortical neurons. However, the effects of osthole on Aβ-induced neurotoxicity in neural cells have rarely been reported. The current study was designed to investigate the protective effects of osthole on a cell model of AD insulted by exogenous Aβ25-35 and the potential mechanism(s). In this study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, immunofluorescence analysis, apoptosis assay, reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) techniques were used in primary cortical neurons and SH-SY5Y cells. Our data showed that osthole reduced intracellular Aβ levels in neural cells, which was associated with decreased BACE1 protein; osthole reversed exogenous Aβ25-35-induced cell viability loss, apoptosis, and synapsin-1 reduction, which was related to the reestablishment of phosphorylation of cyclic AMP response element-binding protein (CREB). The collective evidence indicates that osthole possesses the ability to protect cortical neurons and SH-SY5Y cells against Aβ injury, and the underlying mechanism may be attributed to the enhancement of CREB phosphorylation.</abstract><cop>Japan</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>24432380</pmid><doi>10.1248/bpb.b13-00561</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | J-STAGE Free; MEDLINE; EZB-FREE-00999 freely available EZB journals; Free Full-Text Journals in Chemistry |
| subjects | Alzheimer’s disease Amyloid beta-Peptides - toxicity Amyloid Precursor Protein Secretases - metabolism Animals Aspartic Acid Endopeptidases - metabolism bcl-2-Associated X Protein - genetics Cell Line, Tumor Cells, Cultured Coumarins - pharmacology cyclic AMP response element-binding protein Cyclic AMP Response Element-Binding Protein - genetics Cyclic AMP Response Element-Binding Protein - metabolism Humans Mice Mice, Inbred C57BL Neurons - drug effects Neurons - metabolism Neuroprotective Agents - pharmacology osthole Peptide Fragments - toxicity Phosphorylation - drug effects Proto-Oncogene Proteins c-bcl-2 - genetics Synapsins - metabolism β-amyloid peptide25-35 |
| title | Osthole Reverses Beta-Amyloid Peptide Cytotoxicity on Neural Cells by Enhancing Cyclic AMP Response Element-Binding Protein Phosphorylation |
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