Vitexin prevents Aβ proteotoxicity in transgenic Caenorhabditis elegans model of Alzheimer's disease by modulating unfolded protein response
Alzheimer's disease (AD) accounts for an estimated 60% to 80% of all dementia cases. The present study is aimed at evaluating the neuroprotective efficacy of vitexin, an apigenin flavone glycoside using transgenic Caenorhabditis elegans strain (CL2006) of AD. The neuroprotective effect of vitex...
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| Veröffentlicht in: | Journal of biochemical and molecular toxicology 2021-01, Vol.35 (1), p.e22632-n/a |
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| container_title | Journal of biochemical and molecular toxicology |
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| creator | Malar, Dicson Sheeja Prasanth, Mani Iyer Jeyakumar, Mahalingam Balamurugan, Krishnaswamy Devi, Kasi Pandima |
| description | Alzheimer's disease (AD) accounts for an estimated 60% to 80% of all dementia cases. The present study is aimed at evaluating the neuroprotective efficacy of vitexin, an apigenin flavone glycoside using transgenic Caenorhabditis elegans strain (CL2006) of AD. The neuroprotective effect of vitexin was determined using physiological assays, quantitative polymerase chain reaction, and Western blotting. The results of survival and paralysis assay indicate that vitexin (200 μM) significantly extended the lifespan of the nematodes. Vitexin‐treated nematodes showed a significant reduction in the expression of Aβ, ace‐1, and ace‐2 genes when compared to control. Further, vitexin significantly upregulated the expression of acr‐8 and dnj‐14, and increased the lifespan of the nematodes. Vitexin was also found to modulate the unfolded protein response genes (hsp‐4, pek‐1, ire‐1, and xbp‐1) and suppress the expression of Aβ. Overall, the results show that vitexin acts as a neuroprotective agent and protects transgenic C. elegans strains from Aβ proteotoxicity. |
| doi_str_mv | 10.1002/jbt.22632 |
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The present study is aimed at evaluating the neuroprotective efficacy of vitexin, an apigenin flavone glycoside using transgenic Caenorhabditis elegans strain (CL2006) of AD. The neuroprotective effect of vitexin was determined using physiological assays, quantitative polymerase chain reaction, and Western blotting. The results of survival and paralysis assay indicate that vitexin (200 μM) significantly extended the lifespan of the nematodes. Vitexin‐treated nematodes showed a significant reduction in the expression of Aβ, ace‐1, and ace‐2 genes when compared to control. Further, vitexin significantly upregulated the expression of acr‐8 and dnj‐14, and increased the lifespan of the nematodes. Vitexin was also found to modulate the unfolded protein response genes (hsp‐4, pek‐1, ire‐1, and xbp‐1) and suppress the expression of Aβ. Overall, the results show that vitexin acts as a neuroprotective agent and protects transgenic C. elegans strains from Aβ proteotoxicity.</description><identifier>ISSN: 1095-6670</identifier><identifier>EISSN: 1099-0461</identifier><identifier>DOI: 10.1002/jbt.22632</identifier><identifier>PMID: 32926499</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Alzheimer's disease ; C. elegans ; Caenorhabditis elegans ; Dementia disorders ; dnj‐14 ; Flavone glycosides ; Genes ; Life span ; Nematodes ; Neurodegenerative diseases ; Neuroprotection ; Paralysis ; Physiological effects ; Polymerase chain reaction ; Protein folding ; Proteins ; vitexin ; Western blotting ; Worms</subject><ispartof>Journal of biochemical and molecular toxicology, 2021-01, Vol.35 (1), p.e22632-n/a</ispartof><rights>2020 Wiley Periodicals LLC</rights><rights>2020 Wiley Periodicals LLC.</rights><rights>2021 Wiley Periodicals LLC</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3532-39c3aac2ced01f2da668bb58940b1eb8351679ef818ec2237d89e8b6c954b4533</citedby><cites>FETCH-LOGICAL-c3532-39c3aac2ced01f2da668bb58940b1eb8351679ef818ec2237d89e8b6c954b4533</cites><orcidid>0000-0002-6175-8961</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjbt.22632$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjbt.22632$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32926499$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Malar, Dicson Sheeja</creatorcontrib><creatorcontrib>Prasanth, Mani Iyer</creatorcontrib><creatorcontrib>Jeyakumar, Mahalingam</creatorcontrib><creatorcontrib>Balamurugan, Krishnaswamy</creatorcontrib><creatorcontrib>Devi, Kasi Pandima</creatorcontrib><title>Vitexin prevents Aβ proteotoxicity in transgenic Caenorhabditis elegans model of Alzheimer's disease by modulating unfolded protein response</title><title>Journal of biochemical and molecular toxicology</title><addtitle>J Biochem Mol Toxicol</addtitle><description>Alzheimer's disease (AD) accounts for an estimated 60% to 80% of all dementia cases. The present study is aimed at evaluating the neuroprotective efficacy of vitexin, an apigenin flavone glycoside using transgenic Caenorhabditis elegans strain (CL2006) of AD. The neuroprotective effect of vitexin was determined using physiological assays, quantitative polymerase chain reaction, and Western blotting. The results of survival and paralysis assay indicate that vitexin (200 μM) significantly extended the lifespan of the nematodes. Vitexin‐treated nematodes showed a significant reduction in the expression of Aβ, ace‐1, and ace‐2 genes when compared to control. Further, vitexin significantly upregulated the expression of acr‐8 and dnj‐14, and increased the lifespan of the nematodes. Vitexin was also found to modulate the unfolded protein response genes (hsp‐4, pek‐1, ire‐1, and xbp‐1) and suppress the expression of Aβ. Overall, the results show that vitexin acts as a neuroprotective agent and protects transgenic C. elegans strains from Aβ proteotoxicity.</description><subject>Alzheimer's disease</subject><subject>C. elegans</subject><subject>Caenorhabditis elegans</subject><subject>Dementia disorders</subject><subject>dnj‐14</subject><subject>Flavone glycosides</subject><subject>Genes</subject><subject>Life span</subject><subject>Nematodes</subject><subject>Neurodegenerative diseases</subject><subject>Neuroprotection</subject><subject>Paralysis</subject><subject>Physiological effects</subject><subject>Polymerase chain reaction</subject><subject>Protein folding</subject><subject>Proteins</subject><subject>vitexin</subject><subject>Western blotting</subject><subject>Worms</subject><issn>1095-6670</issn><issn>1099-0461</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp1kctu1DAUhi0EomVgwQsgSywoi7S-xE68HEblpkpsCtvIdk6mHiX2YDulwzvwMjwIz4TbFBZIrHys_9N3jvQj9JySU0oIO9uZfMqY5OwBOqZEqYrUkj68m0UlZUOO0JOUdoQQoRrxGB1xppislTpGP764DDfO432Ea_A54fWvn-UTMoQcbpx1-YBLnKP2aQveWbzR4EO80qZ32SUMI2xLhqfQw4jDgNfj9ytwE8RXCfcugU6AzeE2n0ednd_i2Q9h7KFf9hR7hLQPPsFT9GjQY4Jn9-8KfX57frl5X118evdhs76oLBecVVxZrrVlFnpCB9ZrKVtjRKtqYiiYlgsqGwVDS1uwjPGmbxW0RlolalMLzlfoZPGWA77OkHI3uWRhHLWHMKeO1TVra06IKujLf9BdmKMv1xWqEZKStmxYodcLZWNIKcLQ7aObdDx0lHS3HXWlo-6uo8K-uDfOZoL-L_mnlAKcLcA3N8Lh_6bu45vLRfkbi1KeaQ</recordid><startdate>202101</startdate><enddate>202101</enddate><creator>Malar, Dicson Sheeja</creator><creator>Prasanth, Mani Iyer</creator><creator>Jeyakumar, Mahalingam</creator><creator>Balamurugan, Krishnaswamy</creator><creator>Devi, Kasi Pandima</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6175-8961</orcidid></search><sort><creationdate>202101</creationdate><title>Vitexin prevents Aβ proteotoxicity in transgenic Caenorhabditis elegans model of Alzheimer's disease by modulating unfolded protein response</title><author>Malar, Dicson Sheeja ; Prasanth, Mani Iyer ; Jeyakumar, Mahalingam ; Balamurugan, Krishnaswamy ; Devi, Kasi Pandima</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3532-39c3aac2ced01f2da668bb58940b1eb8351679ef818ec2237d89e8b6c954b4533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Alzheimer's disease</topic><topic>C. elegans</topic><topic>Caenorhabditis elegans</topic><topic>Dementia disorders</topic><topic>dnj‐14</topic><topic>Flavone glycosides</topic><topic>Genes</topic><topic>Life span</topic><topic>Nematodes</topic><topic>Neurodegenerative diseases</topic><topic>Neuroprotection</topic><topic>Paralysis</topic><topic>Physiological effects</topic><topic>Polymerase chain reaction</topic><topic>Protein folding</topic><topic>Proteins</topic><topic>vitexin</topic><topic>Western blotting</topic><topic>Worms</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Malar, Dicson Sheeja</creatorcontrib><creatorcontrib>Prasanth, Mani Iyer</creatorcontrib><creatorcontrib>Jeyakumar, Mahalingam</creatorcontrib><creatorcontrib>Balamurugan, Krishnaswamy</creatorcontrib><creatorcontrib>Devi, Kasi Pandima</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of biochemical and molecular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Malar, Dicson Sheeja</au><au>Prasanth, Mani Iyer</au><au>Jeyakumar, Mahalingam</au><au>Balamurugan, Krishnaswamy</au><au>Devi, Kasi Pandima</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vitexin prevents Aβ proteotoxicity in transgenic Caenorhabditis elegans model of Alzheimer's disease by modulating unfolded protein response</atitle><jtitle>Journal of biochemical and molecular toxicology</jtitle><addtitle>J Biochem Mol Toxicol</addtitle><date>2021-01</date><risdate>2021</risdate><volume>35</volume><issue>1</issue><spage>e22632</spage><epage>n/a</epage><pages>e22632-n/a</pages><issn>1095-6670</issn><eissn>1099-0461</eissn><abstract>Alzheimer's disease (AD) accounts for an estimated 60% to 80% of all dementia cases. The present study is aimed at evaluating the neuroprotective efficacy of vitexin, an apigenin flavone glycoside using transgenic Caenorhabditis elegans strain (CL2006) of AD. The neuroprotective effect of vitexin was determined using physiological assays, quantitative polymerase chain reaction, and Western blotting. The results of survival and paralysis assay indicate that vitexin (200 μM) significantly extended the lifespan of the nematodes. Vitexin‐treated nematodes showed a significant reduction in the expression of Aβ, ace‐1, and ace‐2 genes when compared to control. Further, vitexin significantly upregulated the expression of acr‐8 and dnj‐14, and increased the lifespan of the nematodes. Vitexin was also found to modulate the unfolded protein response genes (hsp‐4, pek‐1, ire‐1, and xbp‐1) and suppress the expression of Aβ. 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| subjects | Alzheimer's disease C. elegans Caenorhabditis elegans Dementia disorders dnj‐14 Flavone glycosides Genes Life span Nematodes Neurodegenerative diseases Neuroprotection Paralysis Physiological effects Polymerase chain reaction Protein folding Proteins vitexin Western blotting Worms |
| title | Vitexin prevents Aβ proteotoxicity in transgenic Caenorhabditis elegans model of Alzheimer's disease by modulating unfolded protein response |
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