Withanone, an Active Constituent from Withania somnifera, Affords Protection Against NMDA-Induced Excitotoxicity in Neuron-Like Cells
Withania somnifera has immense pharmacologic and clinical uses. Owing to its similar pharmacologic activity as that of Korean Ginseng tea, it is popularly called as Indian ginseng. In most cases, extracts of this plant have been evaluated against various diseases or models of disease. However, littl...
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| Veröffentlicht in: | Molecular neurobiology 2017-09, Vol.54 (7), p.5061-5073 |
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| creator | Dar, Nawab John Bhat, Javeed Ahmad Satti, Naresh Kumar Sharma, Parduman Raj Hamid, Abid Ahmad, Muzamil |
| description | Withania somnifera
has immense pharmacologic and clinical uses. Owing to its similar pharmacologic activity as that of Korean Ginseng tea, it is popularly called as Indian ginseng. In most cases, extracts of this plant have been evaluated against various diseases or models of disease. However, little efforts have been made to evaluate individual constituents of this plant for neurodegenerative disorders. Present study was carried out to evaluate Withanone, one of the active constituents of
Withania somnifera
against NMDA-induced excitotoxicity in retinoic acid, differentiated Neuro2a cells. Cells were pre-treated with 5, 10 and 20 μM doses of Withanone and then exposed to 3-mM NMDA for 1 h. MK801, a specific NMDA receptor antagonist, was used as positive control. The results indicated that NMDA induces significant death of cells by accumulation of intracellular Ca
2+
, generation of reactive oxygen species (ROS), loss of mitochondrial membrane potential, crashing of Bax/Bcl-2 ratio, release of cytochrome c, increased caspase expression, induction of lipid peroxidation as measured by malondialdehyde levels and cleavage of poly(ADP-ribose) polymerase-1 (Parp-1), which is indicative of DNA damage. All these parameters were attenuated with various doses of Withanone pre-treatment. These results suggest that Withanone may serve as potential neuroprotective agent. |
| doi_str_mv | 10.1007/s12035-016-0044-7 |
| format | Article |
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has immense pharmacologic and clinical uses. Owing to its similar pharmacologic activity as that of Korean Ginseng tea, it is popularly called as Indian ginseng. In most cases, extracts of this plant have been evaluated against various diseases or models of disease. However, little efforts have been made to evaluate individual constituents of this plant for neurodegenerative disorders. Present study was carried out to evaluate Withanone, one of the active constituents of
Withania somnifera
against NMDA-induced excitotoxicity in retinoic acid, differentiated Neuro2a cells. Cells were pre-treated with 5, 10 and 20 μM doses of Withanone and then exposed to 3-mM NMDA for 1 h. MK801, a specific NMDA receptor antagonist, was used as positive control. The results indicated that NMDA induces significant death of cells by accumulation of intracellular Ca
2+
, generation of reactive oxygen species (ROS), loss of mitochondrial membrane potential, crashing of Bax/Bcl-2 ratio, release of cytochrome c, increased caspase expression, induction of lipid peroxidation as measured by malondialdehyde levels and cleavage of poly(ADP-ribose) polymerase-1 (Parp-1), which is indicative of DNA damage. All these parameters were attenuated with various doses of Withanone pre-treatment. These results suggest that Withanone may serve as potential neuroprotective agent.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-016-0044-7</identifier><identifier>PMID: 27541286</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adenosine diphosphate ; Animals ; Bcl-2 protein ; Biomedical and Life Sciences ; Biomedicine ; Calcium (intracellular) ; Caspase ; Cell Biology ; Cell Differentiation - drug effects ; Cells ; Cytochrome c ; Death ; DNA damage ; Excitotoxicity ; Ginseng ; Glutamic acid receptors (ionotropic) ; Lipid peroxidation ; Malondialdehyde ; Membrane potential ; Membrane Potential, Mitochondrial - drug effects ; Mice ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; N-Methyl-D-aspartic acid receptors ; Neurobiology ; Neurodegenerative diseases ; Neurodegenerative Diseases - drug therapy ; Neurodegenerative Diseases - metabolism ; Neurology ; Neurons ; Neurons - drug effects ; Neurons - metabolism ; Neuroprotection ; Neuroprotective Agents - pharmacology ; Neurosciences ; Peroxidation ; Plant extracts ; Poly(ADP-ribose) ; Poly(ADP-ribose) polymerase ; Poly(ADP-ribose) Polymerases - metabolism ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Receptors, N-Methyl-D-Aspartate - metabolism ; Retinoic acid ; Tea ; Toxicity ; Triterpenes - pharmacology</subject><ispartof>Molecular neurobiology, 2017-09, Vol.54 (7), p.5061-5073</ispartof><rights>Springer Science+Business Media New York 2016</rights><rights>Molecular Neurobiology is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-f93d7472e8688c5077a5161039fd73f3b93bb18fb223d331fedc5ff26f151e8e3</citedby><cites>FETCH-LOGICAL-c372t-f93d7472e8688c5077a5161039fd73f3b93bb18fb223d331fedc5ff26f151e8e3</cites><orcidid>0000-0003-1066-1817</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-016-0044-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-016-0044-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27907,27908,41471,42540,51302</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27541286$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dar, Nawab John</creatorcontrib><creatorcontrib>Bhat, Javeed Ahmad</creatorcontrib><creatorcontrib>Satti, Naresh Kumar</creatorcontrib><creatorcontrib>Sharma, Parduman Raj</creatorcontrib><creatorcontrib>Hamid, Abid</creatorcontrib><creatorcontrib>Ahmad, Muzamil</creatorcontrib><title>Withanone, an Active Constituent from Withania somnifera, Affords Protection Against NMDA-Induced Excitotoxicity in Neuron-Like Cells</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Withania somnifera
has immense pharmacologic and clinical uses. Owing to its similar pharmacologic activity as that of Korean Ginseng tea, it is popularly called as Indian ginseng. In most cases, extracts of this plant have been evaluated against various diseases or models of disease. However, little efforts have been made to evaluate individual constituents of this plant for neurodegenerative disorders. Present study was carried out to evaluate Withanone, one of the active constituents of
Withania somnifera
against NMDA-induced excitotoxicity in retinoic acid, differentiated Neuro2a cells. Cells were pre-treated with 5, 10 and 20 μM doses of Withanone and then exposed to 3-mM NMDA for 1 h. MK801, a specific NMDA receptor antagonist, was used as positive control. The results indicated that NMDA induces significant death of cells by accumulation of intracellular Ca
2+
, generation of reactive oxygen species (ROS), loss of mitochondrial membrane potential, crashing of Bax/Bcl-2 ratio, release of cytochrome c, increased caspase expression, induction of lipid peroxidation as measured by malondialdehyde levels and cleavage of poly(ADP-ribose) polymerase-1 (Parp-1), which is indicative of DNA damage. All these parameters were attenuated with various doses of Withanone pre-treatment. These results suggest that Withanone may serve as potential neuroprotective agent.</description><subject>Adenosine diphosphate</subject><subject>Animals</subject><subject>Bcl-2 protein</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Calcium (intracellular)</subject><subject>Caspase</subject><subject>Cell Biology</subject><subject>Cell Differentiation - drug effects</subject><subject>Cells</subject><subject>Cytochrome c</subject><subject>Death</subject><subject>DNA damage</subject><subject>Excitotoxicity</subject><subject>Ginseng</subject><subject>Glutamic acid receptors (ionotropic)</subject><subject>Lipid peroxidation</subject><subject>Malondialdehyde</subject><subject>Membrane potential</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mice</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>N-Methyl-D-aspartic acid receptors</subject><subject>Neurobiology</subject><subject>Neurodegenerative diseases</subject><subject>Neurodegenerative Diseases - drug therapy</subject><subject>Neurodegenerative Diseases - metabolism</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neurosciences</subject><subject>Peroxidation</subject><subject>Plant extracts</subject><subject>Poly(ADP-ribose)</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors, N-Methyl-D-Aspartate - metabolism</subject><subject>Retinoic acid</subject><subject>Tea</subject><subject>Toxicity</subject><subject>Triterpenes - pharmacology</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kcFuFSEUhonR2Gv1AdwYEjcuinJgGGB5c63a5FpdaFwSZgYq9Q5UYEz7AL63NFONMXF1Fuf7_nOSH6GnQF8CpfJVAUa5IBR6QmnXEXkPbUAITQAUu482VGlOZN-pI_SolEtKGQMqH6IjJkUHTPUb9PNLqF9tTNGdYBvxdqzhh8O7FEsNdXGxYp_TjFcqWFzSHIN32Z7grfcpTwV_zKm65qWmX9jQTHz-_vWWnMVpGd2ET6_HUFNN16HNGxwiPndLTpHsw7d2yh0O5TF64O2huCd38xh9fnP6afeO7D-8Pdtt92TkklXiNZ9kJ5lTvVKjoFJaAT1Qrv0kueeD5sMAyg-M8Ylz8G4ahfes9yDAKceP0Ys19yqn74sr1cyhjO0DG11aigEltGTQd7Shz_9BL9OSY_vOgGZc804DaxSs1JhTKdl5c5XDbPONAWpuOzJrR6Z1ZG47MrI5z-6Sl2F20x_jdykNYCtQ2ipeuPzX6f-m_gJyEZxx</recordid><startdate>20170901</startdate><enddate>20170901</enddate><creator>Dar, Nawab John</creator><creator>Bhat, Javeed Ahmad</creator><creator>Satti, Naresh Kumar</creator><creator>Sharma, Parduman Raj</creator><creator>Hamid, Abid</creator><creator>Ahmad, Muzamil</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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</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>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>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-1066-1817</orcidid></search><sort><creationdate>20170901</creationdate><title>Withanone, an Active Constituent from Withania somnifera, Affords Protection Against NMDA-Induced Excitotoxicity in Neuron-Like Cells</title><author>Dar, Nawab John ; Bhat, Javeed Ahmad ; Satti, Naresh Kumar ; Sharma, Parduman Raj ; Hamid, Abid ; Ahmad, Muzamil</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-f93d7472e8688c5077a5161039fd73f3b93bb18fb223d331fedc5ff26f151e8e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenosine diphosphate</topic><topic>Animals</topic><topic>Bcl-2 protein</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Calcium (intracellular)</topic><topic>Caspase</topic><topic>Cell Biology</topic><topic>Cell Differentiation - drug effects</topic><topic>Cells</topic><topic>Cytochrome c</topic><topic>Death</topic><topic>DNA damage</topic><topic>Excitotoxicity</topic><topic>Ginseng</topic><topic>Glutamic acid receptors (ionotropic)</topic><topic>Lipid peroxidation</topic><topic>Malondialdehyde</topic><topic>Membrane potential</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mice</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>N-Methyl-D-aspartic acid receptors</topic><topic>Neurobiology</topic><topic>Neurodegenerative diseases</topic><topic>Neurodegenerative Diseases - drug therapy</topic><topic>Neurodegenerative Diseases - metabolism</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neurosciences</topic><topic>Peroxidation</topic><topic>Plant extracts</topic><topic>Poly(ADP-ribose)</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptors, N-Methyl-D-Aspartate - metabolism</topic><topic>Retinoic acid</topic><topic>Tea</topic><topic>Toxicity</topic><topic>Triterpenes - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dar, Nawab John</creatorcontrib><creatorcontrib>Bhat, Javeed Ahmad</creatorcontrib><creatorcontrib>Satti, Naresh Kumar</creatorcontrib><creatorcontrib>Sharma, Parduman Raj</creatorcontrib><creatorcontrib>Hamid, Abid</creatorcontrib><creatorcontrib>Ahmad, Muzamil</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>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>Psychology Database (Alumni)</collection><collection>Science 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>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>ProQuest Psychology</collection><collection>Science 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><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dar, Nawab John</au><au>Bhat, Javeed Ahmad</au><au>Satti, Naresh Kumar</au><au>Sharma, Parduman Raj</au><au>Hamid, Abid</au><au>Ahmad, Muzamil</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Withanone, an Active Constituent from Withania somnifera, Affords Protection Against NMDA-Induced Excitotoxicity in Neuron-Like Cells</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2017-09-01</date><risdate>2017</risdate><volume>54</volume><issue>7</issue><spage>5061</spage><epage>5073</epage><pages>5061-5073</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Withania somnifera
has immense pharmacologic and clinical uses. Owing to its similar pharmacologic activity as that of Korean Ginseng tea, it is popularly called as Indian ginseng. In most cases, extracts of this plant have been evaluated against various diseases or models of disease. However, little efforts have been made to evaluate individual constituents of this plant for neurodegenerative disorders. Present study was carried out to evaluate Withanone, one of the active constituents of
Withania somnifera
against NMDA-induced excitotoxicity in retinoic acid, differentiated Neuro2a cells. Cells were pre-treated with 5, 10 and 20 μM doses of Withanone and then exposed to 3-mM NMDA for 1 h. MK801, a specific NMDA receptor antagonist, was used as positive control. The results indicated that NMDA induces significant death of cells by accumulation of intracellular Ca
2+
, generation of reactive oxygen species (ROS), loss of mitochondrial membrane potential, crashing of Bax/Bcl-2 ratio, release of cytochrome c, increased caspase expression, induction of lipid peroxidation as measured by malondialdehyde levels and cleavage of poly(ADP-ribose) polymerase-1 (Parp-1), which is indicative of DNA damage. All these parameters were attenuated with various doses of Withanone pre-treatment. These results suggest that Withanone may serve as potential neuroprotective agent.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>27541286</pmid><doi>10.1007/s12035-016-0044-7</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-1066-1817</orcidid></addata></record> |
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| ispartof | Molecular neurobiology, 2017-09, Vol.54 (7), p.5061-5073 |
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| subjects | Adenosine diphosphate Animals Bcl-2 protein Biomedical and Life Sciences Biomedicine Calcium (intracellular) Caspase Cell Biology Cell Differentiation - drug effects Cells Cytochrome c Death DNA damage Excitotoxicity Ginseng Glutamic acid receptors (ionotropic) Lipid peroxidation Malondialdehyde Membrane potential Membrane Potential, Mitochondrial - drug effects Mice Mitochondria Mitochondria - drug effects Mitochondria - metabolism N-Methyl-D-aspartic acid receptors Neurobiology Neurodegenerative diseases Neurodegenerative Diseases - drug therapy Neurodegenerative Diseases - metabolism Neurology Neurons Neurons - drug effects Neurons - metabolism Neuroprotection Neuroprotective Agents - pharmacology Neurosciences Peroxidation Plant extracts Poly(ADP-ribose) Poly(ADP-ribose) polymerase Poly(ADP-ribose) Polymerases - metabolism Reactive oxygen species Reactive Oxygen Species - metabolism Receptors, N-Methyl-D-Aspartate - metabolism Retinoic acid Tea Toxicity Triterpenes - pharmacology |
| title | Withanone, an Active Constituent from Withania somnifera, Affords Protection Against NMDA-Induced Excitotoxicity in Neuron-Like Cells |
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