Aloysia gratissima prevents cellular damage induced by glutamatergic excitotoxicity
Objectives Aloysia gratissima aqueous extract (AE) was investigated as a putative protective agent against quinolinic acid (QA)‐induced seizures in mice and hippocampal cell damage. Additionally, AE and ferulic acid (FA), the major compound of AE, were tested against neurotoxicity evoked by glutamat...
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| Veröffentlicht in: | Journal of pharmacy and pharmacology 2014-09, Vol.66 (9), p.1294-1302 |
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| container_title | Journal of pharmacy and pharmacology |
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| creator | Zeni, Ana L. B. Vandresen-Filho, Samuel Dal-Cim, Tharine Martins, Wagner C. Bertoldo, Daniela B. Maraschin, Marcelo Tasca, Carla I. |
| description | Objectives
Aloysia gratissima aqueous extract (AE) was investigated as a putative protective agent against quinolinic acid (QA)‐induced seizures in mice and hippocampal cell damage. Additionally, AE and ferulic acid (FA), the major compound of AE, were tested against neurotoxicity evoked by glutamate or its N‐methyl‐D‐aspartate receptor (NMDAR) agonist, QA on hippocampal slices, in vitro.
Methods
Mice were treated with AE before QA infusion (36.8 nmol/site) and seizures were analysed. Cellular viability and modulation of excitatory amino acid transport were verified in hippocampal slices. In‐vitro AE or FA was tested against neurotoxicity induced by glutamate or QA.
Key findings
AE did not prevent QA‐induced seizures; however, it prevented cellular death and disruption of excitatory amino acid transport. In‐vitro AE (0.1 or 1.0 mg/ml) or FA (1 or 10 μm), improved cell viability against citotoxicity exerted by glutamate or QA, respectively. Both AE and FA have protective effects depending on activation of the phosphatidylinositol‐3 kinase (PI3K) signalling pathway.
Conclusions
AE attenuated QA‐induced cell damage possibly involving the glutamate transport modulation through NMDAR interaction. FA shows a similar profile of neuroprotection promoted by AE. Therefore, AE treatment might be a useful strategy in preventing brain damage caused by exacerbation of glutamatergic toxicity in nervous system disorders. |
| doi_str_mv | 10.1111/jphp.12250 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1553232635</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3402909521</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5010-37dcc5d9c9a19396160abb3ddb7647a629de1020814ea332ce6a762ffd4acad33</originalsourceid><addsrcrecordid>eNp9kF9PwjAUxRujEURf_ABmiW8mw_5ZW_ZIUEFFJQGDb03XFiwONttN2bd3iPDofTnJze-cm3sAOEewjeq5XuTveRthTOEBaGIY4ZAj2jkETQgxDgnlpAFOvF9ACDlj7Bg0cMQh7zDYBONumlXeymDuZGG9t0sZ5M58mVXhA2XStEylC7RcyrkJ7EqXyuggqYJ5Whb1sjBublVg1soWWZGtba3VKTiaydSbsz9tgde720lvEA5f-ve97jBUFCIYEq6VojpWsUQxiRliUCYJ0TrhLOKS4VgbBDHsoMhIQrAyTHKGZzMdSSU1IS1wuc3NXfZZGl-IRVa6VX1SIEoJJpgRWlNXW0q5zHtnZiJ39ZeuEgiKTX9i05_47a-GL_4iy2Rp9B7dFVYDaAt829RU_0SJh9FgtAsNtx7rC7Pee6T7EIwTTsX0uS-mk7enxxs8EGPyAxAOi3s</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1553232635</pqid></control><display><type>article</type><title>Aloysia gratissima prevents cellular damage induced by glutamatergic excitotoxicity</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Oxford University Press Journals All Titles (1996-Current)</source><creator>Zeni, Ana L. B. ; Vandresen-Filho, Samuel ; Dal-Cim, Tharine ; Martins, Wagner C. ; Bertoldo, Daniela B. ; Maraschin, Marcelo ; Tasca, Carla I.</creator><creatorcontrib>Zeni, Ana L. B. ; Vandresen-Filho, Samuel ; Dal-Cim, Tharine ; Martins, Wagner C. ; Bertoldo, Daniela B. ; Maraschin, Marcelo ; Tasca, Carla I.</creatorcontrib><description>Objectives
Aloysia gratissima aqueous extract (AE) was investigated as a putative protective agent against quinolinic acid (QA)‐induced seizures in mice and hippocampal cell damage. Additionally, AE and ferulic acid (FA), the major compound of AE, were tested against neurotoxicity evoked by glutamate or its N‐methyl‐D‐aspartate receptor (NMDAR) agonist, QA on hippocampal slices, in vitro.
Methods
Mice were treated with AE before QA infusion (36.8 nmol/site) and seizures were analysed. Cellular viability and modulation of excitatory amino acid transport were verified in hippocampal slices. In‐vitro AE or FA was tested against neurotoxicity induced by glutamate or QA.
Key findings
AE did not prevent QA‐induced seizures; however, it prevented cellular death and disruption of excitatory amino acid transport. In‐vitro AE (0.1 or 1.0 mg/ml) or FA (1 or 10 μm), improved cell viability against citotoxicity exerted by glutamate or QA, respectively. Both AE and FA have protective effects depending on activation of the phosphatidylinositol‐3 kinase (PI3K) signalling pathway.
Conclusions
AE attenuated QA‐induced cell damage possibly involving the glutamate transport modulation through NMDAR interaction. FA shows a similar profile of neuroprotection promoted by AE. Therefore, AE treatment might be a useful strategy in preventing brain damage caused by exacerbation of glutamatergic toxicity in nervous system disorders.</description><identifier>ISSN: 0022-3573</identifier><identifier>EISSN: 2042-7158</identifier><identifier>DOI: 10.1111/jphp.12250</identifier><identifier>PMID: 24707860</identifier><identifier>CODEN: JPPMAB</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Aloysia gratissima ; Animals ; Biological Transport ; Cell Death - drug effects ; Cell Survival - drug effects ; cell viability ; Coumaric Acids - pharmacology ; Coumaric Acids - therapeutic use ; Excitatory Amino Acid Agonists - adverse effects ; Excitatory Amino Acids - metabolism ; ferulic acid ; Glutamic Acid - adverse effects ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hippocampus - pathology ; Male ; Mice, Inbred Strains ; neuroprotection ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Neurotoxicity Syndromes - drug therapy ; Neurotoxicity Syndromes - metabolism ; Neurotoxicity Syndromes - pathology ; Phosphatidylinositol 3-Kinase - metabolism ; Phytotherapy ; Plant Extracts - pharmacology ; Plant Extracts - therapeutic use ; quinolinic acid ; Quinolinic Acid - adverse effects ; Receptors, N-Methyl-D-Aspartate - agonists ; Seizures - chemically induced ; Seizures - metabolism ; Verbenaceae - chemistry</subject><ispartof>Journal of pharmacy and pharmacology, 2014-09, Vol.66 (9), p.1294-1302</ispartof><rights>2014 Royal Pharmaceutical Society</rights><rights>2014 Royal Pharmaceutical Society.</rights><rights>Copyright © 2014 Royal Pharmaceutical Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5010-37dcc5d9c9a19396160abb3ddb7647a629de1020814ea332ce6a762ffd4acad33</citedby><cites>FETCH-LOGICAL-c5010-37dcc5d9c9a19396160abb3ddb7647a629de1020814ea332ce6a762ffd4acad33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjphp.12250$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjphp.12250$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24707860$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zeni, Ana L. B.</creatorcontrib><creatorcontrib>Vandresen-Filho, Samuel</creatorcontrib><creatorcontrib>Dal-Cim, Tharine</creatorcontrib><creatorcontrib>Martins, Wagner C.</creatorcontrib><creatorcontrib>Bertoldo, Daniela B.</creatorcontrib><creatorcontrib>Maraschin, Marcelo</creatorcontrib><creatorcontrib>Tasca, Carla I.</creatorcontrib><title>Aloysia gratissima prevents cellular damage induced by glutamatergic excitotoxicity</title><title>Journal of pharmacy and pharmacology</title><addtitle>J Pharm Pharmacol</addtitle><description>Objectives
Aloysia gratissima aqueous extract (AE) was investigated as a putative protective agent against quinolinic acid (QA)‐induced seizures in mice and hippocampal cell damage. Additionally, AE and ferulic acid (FA), the major compound of AE, were tested against neurotoxicity evoked by glutamate or its N‐methyl‐D‐aspartate receptor (NMDAR) agonist, QA on hippocampal slices, in vitro.
Methods
Mice were treated with AE before QA infusion (36.8 nmol/site) and seizures were analysed. Cellular viability and modulation of excitatory amino acid transport were verified in hippocampal slices. In‐vitro AE or FA was tested against neurotoxicity induced by glutamate or QA.
Key findings
AE did not prevent QA‐induced seizures; however, it prevented cellular death and disruption of excitatory amino acid transport. In‐vitro AE (0.1 or 1.0 mg/ml) or FA (1 or 10 μm), improved cell viability against citotoxicity exerted by glutamate or QA, respectively. Both AE and FA have protective effects depending on activation of the phosphatidylinositol‐3 kinase (PI3K) signalling pathway.
Conclusions
AE attenuated QA‐induced cell damage possibly involving the glutamate transport modulation through NMDAR interaction. FA shows a similar profile of neuroprotection promoted by AE. Therefore, AE treatment might be a useful strategy in preventing brain damage caused by exacerbation of glutamatergic toxicity in nervous system disorders.</description><subject>Aloysia gratissima</subject><subject>Animals</subject><subject>Biological Transport</subject><subject>Cell Death - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>cell viability</subject><subject>Coumaric Acids - pharmacology</subject><subject>Coumaric Acids - therapeutic use</subject><subject>Excitatory Amino Acid Agonists - adverse effects</subject><subject>Excitatory Amino Acids - metabolism</subject><subject>ferulic acid</subject><subject>Glutamic Acid - adverse effects</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Male</subject><subject>Mice, Inbred Strains</subject><subject>neuroprotection</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Neurotoxicity Syndromes - drug therapy</subject><subject>Neurotoxicity Syndromes - metabolism</subject><subject>Neurotoxicity Syndromes - pathology</subject><subject>Phosphatidylinositol 3-Kinase - metabolism</subject><subject>Phytotherapy</subject><subject>Plant Extracts - pharmacology</subject><subject>Plant Extracts - therapeutic use</subject><subject>quinolinic acid</subject><subject>Quinolinic Acid - adverse effects</subject><subject>Receptors, N-Methyl-D-Aspartate - agonists</subject><subject>Seizures - chemically induced</subject><subject>Seizures - metabolism</subject><subject>Verbenaceae - chemistry</subject><issn>0022-3573</issn><issn>2042-7158</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kF9PwjAUxRujEURf_ABmiW8mw_5ZW_ZIUEFFJQGDb03XFiwONttN2bd3iPDofTnJze-cm3sAOEewjeq5XuTveRthTOEBaGIY4ZAj2jkETQgxDgnlpAFOvF9ACDlj7Bg0cMQh7zDYBONumlXeymDuZGG9t0sZ5M58mVXhA2XStEylC7RcyrkJ7EqXyuggqYJ5Whb1sjBublVg1soWWZGtba3VKTiaydSbsz9tgde720lvEA5f-ve97jBUFCIYEq6VojpWsUQxiRliUCYJ0TrhLOKS4VgbBDHsoMhIQrAyTHKGZzMdSSU1IS1wuc3NXfZZGl-IRVa6VX1SIEoJJpgRWlNXW0q5zHtnZiJ39ZeuEgiKTX9i05_47a-GL_4iy2Rp9B7dFVYDaAt829RU_0SJh9FgtAsNtx7rC7Pee6T7EIwTTsX0uS-mk7enxxs8EGPyAxAOi3s</recordid><startdate>201409</startdate><enddate>201409</enddate><creator>Zeni, Ana L. B.</creator><creator>Vandresen-Filho, Samuel</creator><creator>Dal-Cim, Tharine</creator><creator>Martins, Wagner C.</creator><creator>Bertoldo, Daniela B.</creator><creator>Maraschin, Marcelo</creator><creator>Tasca, Carla I.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7QP</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope></search><sort><creationdate>201409</creationdate><title>Aloysia gratissima prevents cellular damage induced by glutamatergic excitotoxicity</title><author>Zeni, Ana L. B. ; Vandresen-Filho, Samuel ; Dal-Cim, Tharine ; Martins, Wagner C. ; Bertoldo, Daniela B. ; Maraschin, Marcelo ; Tasca, Carla I.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5010-37dcc5d9c9a19396160abb3ddb7647a629de1020814ea332ce6a762ffd4acad33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aloysia gratissima</topic><topic>Animals</topic><topic>Biological Transport</topic><topic>Cell Death - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>cell viability</topic><topic>Coumaric Acids - pharmacology</topic><topic>Coumaric Acids - therapeutic use</topic><topic>Excitatory Amino Acid Agonists - adverse effects</topic><topic>Excitatory Amino Acids - metabolism</topic><topic>ferulic acid</topic><topic>Glutamic Acid - adverse effects</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - pathology</topic><topic>Male</topic><topic>Mice, Inbred Strains</topic><topic>neuroprotection</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Neurotoxicity Syndromes - drug therapy</topic><topic>Neurotoxicity Syndromes - metabolism</topic><topic>Neurotoxicity Syndromes - pathology</topic><topic>Phosphatidylinositol 3-Kinase - metabolism</topic><topic>Phytotherapy</topic><topic>Plant Extracts - pharmacology</topic><topic>Plant Extracts - therapeutic use</topic><topic>quinolinic acid</topic><topic>Quinolinic Acid - adverse effects</topic><topic>Receptors, N-Methyl-D-Aspartate - agonists</topic><topic>Seizures - chemically induced</topic><topic>Seizures - metabolism</topic><topic>Verbenaceae - chemistry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zeni, Ana L. B.</creatorcontrib><creatorcontrib>Vandresen-Filho, Samuel</creatorcontrib><creatorcontrib>Dal-Cim, Tharine</creatorcontrib><creatorcontrib>Martins, Wagner C.</creatorcontrib><creatorcontrib>Bertoldo, Daniela B.</creatorcontrib><creatorcontrib>Maraschin, Marcelo</creatorcontrib><creatorcontrib>Tasca, Carla I.</creatorcontrib><collection>Istex</collection><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>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><jtitle>Journal of pharmacy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeni, Ana L. B.</au><au>Vandresen-Filho, Samuel</au><au>Dal-Cim, Tharine</au><au>Martins, Wagner C.</au><au>Bertoldo, Daniela B.</au><au>Maraschin, Marcelo</au><au>Tasca, Carla I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aloysia gratissima prevents cellular damage induced by glutamatergic excitotoxicity</atitle><jtitle>Journal of pharmacy and pharmacology</jtitle><addtitle>J Pharm Pharmacol</addtitle><date>2014-09</date><risdate>2014</risdate><volume>66</volume><issue>9</issue><spage>1294</spage><epage>1302</epage><pages>1294-1302</pages><issn>0022-3573</issn><eissn>2042-7158</eissn><coden>JPPMAB</coden><abstract>Objectives
Aloysia gratissima aqueous extract (AE) was investigated as a putative protective agent against quinolinic acid (QA)‐induced seizures in mice and hippocampal cell damage. Additionally, AE and ferulic acid (FA), the major compound of AE, were tested against neurotoxicity evoked by glutamate or its N‐methyl‐D‐aspartate receptor (NMDAR) agonist, QA on hippocampal slices, in vitro.
Methods
Mice were treated with AE before QA infusion (36.8 nmol/site) and seizures were analysed. Cellular viability and modulation of excitatory amino acid transport were verified in hippocampal slices. In‐vitro AE or FA was tested against neurotoxicity induced by glutamate or QA.
Key findings
AE did not prevent QA‐induced seizures; however, it prevented cellular death and disruption of excitatory amino acid transport. In‐vitro AE (0.1 or 1.0 mg/ml) or FA (1 or 10 μm), improved cell viability against citotoxicity exerted by glutamate or QA, respectively. Both AE and FA have protective effects depending on activation of the phosphatidylinositol‐3 kinase (PI3K) signalling pathway.
Conclusions
AE attenuated QA‐induced cell damage possibly involving the glutamate transport modulation through NMDAR interaction. FA shows a similar profile of neuroprotection promoted by AE. Therefore, AE treatment might be a useful strategy in preventing brain damage caused by exacerbation of glutamatergic toxicity in nervous system disorders.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>24707860</pmid><doi>10.1111/jphp.12250</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Oxford University Press Journals All Titles (1996-Current) |
| subjects | Aloysia gratissima Animals Biological Transport Cell Death - drug effects Cell Survival - drug effects cell viability Coumaric Acids - pharmacology Coumaric Acids - therapeutic use Excitatory Amino Acid Agonists - adverse effects Excitatory Amino Acids - metabolism ferulic acid Glutamic Acid - adverse effects Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology Male Mice, Inbred Strains neuroprotection Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Neurotoxicity Syndromes - drug therapy Neurotoxicity Syndromes - metabolism Neurotoxicity Syndromes - pathology Phosphatidylinositol 3-Kinase - metabolism Phytotherapy Plant Extracts - pharmacology Plant Extracts - therapeutic use quinolinic acid Quinolinic Acid - adverse effects Receptors, N-Methyl-D-Aspartate - agonists Seizures - chemically induced Seizures - metabolism Verbenaceae - chemistry |
| title | Aloysia gratissima prevents cellular damage induced by glutamatergic excitotoxicity |
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