Inhibitory Effects of Edaravone in β-Amyloid-Induced Neurotoxicity in Rats
Amyloid protein can damage nerve cells through a variety of biological mechanisms including oxidative stress, alterations in calcium homeostasis, and proapoptosis. Edaravone, a potent free radical scavenger possessing antioxidant effects, has been proved neuroprotective effect in stroke patients. Th...
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| description | Amyloid protein can damage nerve cells through a variety of biological mechanisms including oxidative stress, alterations in calcium homeostasis, and proapoptosis. Edaravone, a potent free radical scavenger possessing antioxidant effects, has been proved neuroprotective effect in stroke patients. The current study aimed to investigate the effects of EDA in an Aβ-induced rat model of AD, by studying Aβ1–40-induced voltage-gated calcium channel currents in hippocampal CA1 pyramidal neurons, learning and memory behavioral tests, the number of surviving cholinergic neurons in the basal forebrain, and the acetylcholine level in the hippocampus in this rat model of AD. The results showed that the Aβ1–40-induced increase of ICa can be inhibited by EDA in a dose-dependent manner. Treatment with EDA significantly improved Aβ1–40-induced learning and memory performance. Choline acetyltransferase positive cells in basal forebrain and acetylcholine content in the hippocampus were increased by the administration of EDA as compared with the non-EDA treated Aβ1–40 group. These results demonstrate that EDA can inhibit the neurotoxic effect of Aβ toxicity. Collectively, these findings suggest that EDA may serve as a potential complemental treatment strategy for AD. |
| doi_str_mv | 10.1155/2014/370368 |
| format | Article |
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Edaravone, a potent free radical scavenger possessing antioxidant effects, has been proved neuroprotective effect in stroke patients. The current study aimed to investigate the effects of EDA in an Aβ-induced rat model of AD, by studying Aβ1–40-induced voltage-gated calcium channel currents in hippocampal CA1 pyramidal neurons, learning and memory behavioral tests, the number of surviving cholinergic neurons in the basal forebrain, and the acetylcholine level in the hippocampus in this rat model of AD. The results showed that the Aβ1–40-induced increase of ICa can be inhibited by EDA in a dose-dependent manner. Treatment with EDA significantly improved Aβ1–40-induced learning and memory performance. Choline acetyltransferase positive cells in basal forebrain and acetylcholine content in the hippocampus were increased by the administration of EDA as compared with the non-EDA treated Aβ1–40 group. These results demonstrate that EDA can inhibit the neurotoxic effect of Aβ toxicity. Collectively, these findings suggest that EDA may serve as a potential complemental treatment strategy for AD.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2014/370368</identifier><identifier>PMID: 24804216</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Puplishing Corporation</publisher><subject>Alzheimer Disease - chemically induced ; Alzheimer Disease - drug therapy ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Alzheimer's disease ; Amyloid beta-Peptides - toxicity ; Animals ; Antipyrine - analogs & derivatives ; Antipyrine - pharmacology ; CA1 Region, Hippocampal - metabolism ; CA1 Region, Hippocampal - pathology ; Care and treatment ; Disease Models, Animal ; Drug therapy ; Free Radical Scavengers - pharmacology ; Learning - drug effects ; Male ; Medical research ; Medicine, Experimental ; Memory - drug effects ; Neurotoxic agents ; Neurotoxicity Syndromes - drug therapy ; Neurotoxicity Syndromes - metabolism ; Neurotoxicity Syndromes - pathology ; Oxidative stress ; Peptide Fragments - toxicity ; Rats ; Rats, Sprague-Dawley</subject><ispartof>BioMed research international, 2014-01, Vol.2014 (2014), p.1-7</ispartof><rights>Copyright © 2014 Feng He et al.</rights><rights>COPYRIGHT 2014 John Wiley & Sons, Inc.</rights><rights>Copyright © 2014 Feng He et al. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-a655e4fc2caecd1ca407d02c62594682034498a7249ff6864f77e72e80ae7b743</citedby><cites>FETCH-LOGICAL-c499t-a655e4fc2caecd1ca407d02c62594682034498a7249ff6864f77e72e80ae7b743</cites><orcidid>0000-0001-9202-5878</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3996961/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3996961/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24804216$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Yu, Jin-Tai</contributor><creatorcontrib>He, Feng</creatorcontrib><creatorcontrib>Cao, Yan-Ping</creatorcontrib><creatorcontrib>Che, Feng-Yuan</creatorcontrib><creatorcontrib>Yang, Lian-Hong</creatorcontrib><creatorcontrib>Xiao, Song-Hua</creatorcontrib><creatorcontrib>Liu, Jun</creatorcontrib><title>Inhibitory Effects of Edaravone in β-Amyloid-Induced Neurotoxicity in Rats</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Amyloid protein can damage nerve cells through a variety of biological mechanisms including oxidative stress, alterations in calcium homeostasis, and proapoptosis. Edaravone, a potent free radical scavenger possessing antioxidant effects, has been proved neuroprotective effect in stroke patients. The current study aimed to investigate the effects of EDA in an Aβ-induced rat model of AD, by studying Aβ1–40-induced voltage-gated calcium channel currents in hippocampal CA1 pyramidal neurons, learning and memory behavioral tests, the number of surviving cholinergic neurons in the basal forebrain, and the acetylcholine level in the hippocampus in this rat model of AD. The results showed that the Aβ1–40-induced increase of ICa can be inhibited by EDA in a dose-dependent manner. Treatment with EDA significantly improved Aβ1–40-induced learning and memory performance. Choline acetyltransferase positive cells in basal forebrain and acetylcholine content in the hippocampus were increased by the administration of EDA as compared with the non-EDA treated Aβ1–40 group. These results demonstrate that EDA can inhibit the neurotoxic effect of Aβ toxicity. Collectively, these findings suggest that EDA may serve as a potential complemental treatment strategy for AD.</description><subject>Alzheimer Disease - chemically induced</subject><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - toxicity</subject><subject>Animals</subject><subject>Antipyrine - analogs & derivatives</subject><subject>Antipyrine - pharmacology</subject><subject>CA1 Region, Hippocampal - metabolism</subject><subject>CA1 Region, Hippocampal - pathology</subject><subject>Care and treatment</subject><subject>Disease Models, Animal</subject><subject>Drug therapy</subject><subject>Free Radical Scavengers - pharmacology</subject><subject>Learning - drug effects</subject><subject>Male</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Memory - drug effects</subject><subject>Neurotoxic agents</subject><subject>Neurotoxicity Syndromes - drug therapy</subject><subject>Neurotoxicity Syndromes - metabolism</subject><subject>Neurotoxicity Syndromes - pathology</subject><subject>Oxidative stress</subject><subject>Peptide Fragments - toxicity</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><recordid>eNqF0U1rFDEYB_Agii1rTz0rA16kMjZvk5eLsJStXVpaEHsO2cyTbmQ2qclMdb-WH8TP1FmmXfRkLgnkx5-H54_QMcGfCGmaU4oJP2USM6FeoEPKCK8F4eTl_s3YAToq5TsejyICa_EaHVCuMKdEHKLLZVyHVehT3lYL78H1pUq-WrQ224cUoQqx-vO7nm-2XQptvYzt4KCtrmHIqU-_ggv9dme-2r68Qa-87QocPd0zdHu--HZ2UV_dfFmeza9qx7XuayuaBrh31FlwLXGWY9li6gRtNBeKYsa5VlZSrr0XSnAvJUgKCluQK8nZDH2ecu-H1QZaB7HPtjP3OWxs3ppkg_n3J4a1uUsPhmkt9LiSGfrwFJDTjwFKbzahOOg6GyENxZCGat1I0eiRvp_one3AhOjTmOh23Mw5lZhSqeioPk7K5VRKBr8fhmCz68nsejJTT6N-9_f8e_vcyghOJrAOsbU_w3_S3k4YRgLe7jEXQnDFHgGC76NA</recordid><startdate>20140101</startdate><enddate>20140101</enddate><creator>He, Feng</creator><creator>Cao, Yan-Ping</creator><creator>Che, Feng-Yuan</creator><creator>Yang, Lian-Hong</creator><creator>Xiao, Song-Hua</creator><creator>Liu, Jun</creator><general>Hindawi Puplishing Corporation</general><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7QO</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9202-5878</orcidid></search><sort><creationdate>20140101</creationdate><title>Inhibitory Effects of Edaravone in β-Amyloid-Induced Neurotoxicity in Rats</title><author>He, Feng ; Cao, Yan-Ping ; Che, Feng-Yuan ; Yang, Lian-Hong ; Xiao, Song-Hua ; Liu, Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-a655e4fc2caecd1ca407d02c62594682034498a7249ff6864f77e72e80ae7b743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Alzheimer Disease - chemically induced</topic><topic>Alzheimer Disease - drug therapy</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - toxicity</topic><topic>Animals</topic><topic>Antipyrine - analogs & derivatives</topic><topic>Antipyrine - pharmacology</topic><topic>CA1 Region, Hippocampal - metabolism</topic><topic>CA1 Region, Hippocampal - pathology</topic><topic>Care and treatment</topic><topic>Disease Models, Animal</topic><topic>Drug therapy</topic><topic>Free Radical Scavengers - pharmacology</topic><topic>Learning - drug effects</topic><topic>Male</topic><topic>Medical research</topic><topic>Medicine, Experimental</topic><topic>Memory - drug effects</topic><topic>Neurotoxic agents</topic><topic>Neurotoxicity Syndromes - drug therapy</topic><topic>Neurotoxicity Syndromes - metabolism</topic><topic>Neurotoxicity Syndromes - pathology</topic><topic>Oxidative stress</topic><topic>Peptide Fragments - toxicity</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>He, Feng</creatorcontrib><creatorcontrib>Cao, Yan-Ping</creatorcontrib><creatorcontrib>Che, Feng-Yuan</creatorcontrib><creatorcontrib>Yang, Lian-Hong</creatorcontrib><creatorcontrib>Xiao, Song-Hua</creatorcontrib><creatorcontrib>Liu, Jun</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, Feng</au><au>Cao, Yan-Ping</au><au>Che, Feng-Yuan</au><au>Yang, Lian-Hong</au><au>Xiao, Song-Hua</au><au>Liu, Jun</au><au>Yu, Jin-Tai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibitory Effects of Edaravone in β-Amyloid-Induced Neurotoxicity in Rats</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2014-01-01</date><risdate>2014</risdate><volume>2014</volume><issue>2014</issue><spage>1</spage><epage>7</epage><pages>1-7</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Amyloid protein can damage nerve cells through a variety of biological mechanisms including oxidative stress, alterations in calcium homeostasis, and proapoptosis. Edaravone, a potent free radical scavenger possessing antioxidant effects, has been proved neuroprotective effect in stroke patients. The current study aimed to investigate the effects of EDA in an Aβ-induced rat model of AD, by studying Aβ1–40-induced voltage-gated calcium channel currents in hippocampal CA1 pyramidal neurons, learning and memory behavioral tests, the number of surviving cholinergic neurons in the basal forebrain, and the acetylcholine level in the hippocampus in this rat model of AD. The results showed that the Aβ1–40-induced increase of ICa can be inhibited by EDA in a dose-dependent manner. Treatment with EDA significantly improved Aβ1–40-induced learning and memory performance. Choline acetyltransferase positive cells in basal forebrain and acetylcholine content in the hippocampus were increased by the administration of EDA as compared with the non-EDA treated Aβ1–40 group. These results demonstrate that EDA can inhibit the neurotoxic effect of Aβ toxicity. Collectively, these findings suggest that EDA may serve as a potential complemental treatment strategy for AD.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Puplishing Corporation</pub><pmid>24804216</pmid><doi>10.1155/2014/370368</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0001-9202-5878</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Alzheimer Disease - chemically induced Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - toxicity Animals Antipyrine - analogs & derivatives Antipyrine - pharmacology CA1 Region, Hippocampal - metabolism CA1 Region, Hippocampal - pathology Care and treatment Disease Models, Animal Drug therapy Free Radical Scavengers - pharmacology Learning - drug effects Male Medical research Medicine, Experimental Memory - drug effects Neurotoxic agents Neurotoxicity Syndromes - drug therapy Neurotoxicity Syndromes - metabolism Neurotoxicity Syndromes - pathology Oxidative stress Peptide Fragments - toxicity Rats Rats, Sprague-Dawley |
| title | Inhibitory Effects of Edaravone in β-Amyloid-Induced Neurotoxicity in Rats |
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