Albicanol Alleviates D-Galactose-Induced Aging and Improves Behavioral Ability Via by Alleviating Oxidative Stress-Induced Damage
Albicanol is a natural terpenoid derived from Dryopteris fragrans . Herein, we assessed the ability of Albicanol to protect against oxidative stress-induced senescence. Using a murine model of D-galactose (D-gal)-induced aging, we determined that Albicanol treatment can reverse D-gal-mediated learni...
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| Veröffentlicht in: | Neurochemical research 2021-05, Vol.46 (5), p.1058-1067 |
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| creator | Chen, Ling Ling Zhang, Dong Rui Li, Jie Wang, He Meng Song, Chun Hua Tang, Xun Guan, Yalin Chang, Ying Wang, Wen Fei |
| description | Albicanol is a natural terpenoid derived from
Dryopteris fragrans
. Herein, we assessed the ability of Albicanol to protect against oxidative stress-induced senescence. Using a murine model of D-galactose (D-gal)-induced aging, we determined that Albicanol treatment can reverse D-gal-mediated learning impairments and behavioral changes, while also remediating brain tissue damage in treated mice. We found that serum SOD, CAT, GSH-Px, and T-AOC levels were significantly decreased in aging mice, and that Albicanol treatment significantly increased the serum levels of these antioxidant enzymes. We additionally evaluated the impact of Albicanol treatment on the Keap1/Nrf2/ARE signaling pathway, and found that it was able to decrease Keap1 expression while increasing the expression of Nrf2, thereby activating this signaling pathway, suppressing oxidative damage, and enhancing the expression of downstream target genes including SOD, GSH, GST, HO-1, and NQO1 in this murine aging model system. Albicanol treatment also inhibited the secretion of inflammatory TNF-a and IL-1b. Together, these data indicated that Albicanol can activate Nrf2 pathway-related genes, thereby inhibition of delayed aging by alleviating oxidative stress-induced damage. |
| doi_str_mv | 10.1007/s11064-020-03220-x |
| format | Article |
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Dryopteris fragrans
. Herein, we assessed the ability of Albicanol to protect against oxidative stress-induced senescence. Using a murine model of D-galactose (D-gal)-induced aging, we determined that Albicanol treatment can reverse D-gal-mediated learning impairments and behavioral changes, while also remediating brain tissue damage in treated mice. We found that serum SOD, CAT, GSH-Px, and T-AOC levels were significantly decreased in aging mice, and that Albicanol treatment significantly increased the serum levels of these antioxidant enzymes. We additionally evaluated the impact of Albicanol treatment on the Keap1/Nrf2/ARE signaling pathway, and found that it was able to decrease Keap1 expression while increasing the expression of Nrf2, thereby activating this signaling pathway, suppressing oxidative damage, and enhancing the expression of downstream target genes including SOD, GSH, GST, HO-1, and NQO1 in this murine aging model system. Albicanol treatment also inhibited the secretion of inflammatory TNF-a and IL-1b. Together, these data indicated that Albicanol can activate Nrf2 pathway-related genes, thereby inhibition of delayed aging by alleviating oxidative stress-induced damage.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-020-03220-x</identifier><identifier>PMID: 33761044</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Aging ; Aging (artificial) ; Aging (natural) ; Animal models ; Animal tissues ; Antioxidants ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Brain damage ; Brain injury ; Cell Biology ; D-Galactose ; Galactose ; Gene expression ; Genes ; IL-1β ; Inflammation ; Interleukin 1 ; Model testing ; Neurochemistry ; Neurology ; Neurosciences ; Original Paper ; Oxidative stress ; Senescence ; Serum levels ; Signal transduction ; Signaling ; Tumor necrosis factor-α</subject><ispartof>Neurochemical research, 2021-05, Vol.46 (5), p.1058-1067</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature 2021</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-fe8967fb0d6f6f263603752743ff8639cbc0817ce3c8119302c433378c63644f3</citedby><cites>FETCH-LOGICAL-c375t-fe8967fb0d6f6f263603752743ff8639cbc0817ce3c8119302c433378c63644f3</cites><orcidid>0000-0001-6884-5585</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/s11064-020-03220-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11064-020-03220-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33761044$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Ling Ling</creatorcontrib><creatorcontrib>Zhang, Dong Rui</creatorcontrib><creatorcontrib>Li, Jie</creatorcontrib><creatorcontrib>Wang, He Meng</creatorcontrib><creatorcontrib>Song, Chun Hua</creatorcontrib><creatorcontrib>Tang, Xun</creatorcontrib><creatorcontrib>Guan, Yalin</creatorcontrib><creatorcontrib>Chang, Ying</creatorcontrib><creatorcontrib>Wang, Wen Fei</creatorcontrib><title>Albicanol Alleviates D-Galactose-Induced Aging and Improves Behavioral Ability Via by Alleviating Oxidative Stress-Induced Damage</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>Albicanol is a natural terpenoid derived from
Dryopteris fragrans
. Herein, we assessed the ability of Albicanol to protect against oxidative stress-induced senescence. Using a murine model of D-galactose (D-gal)-induced aging, we determined that Albicanol treatment can reverse D-gal-mediated learning impairments and behavioral changes, while also remediating brain tissue damage in treated mice. We found that serum SOD, CAT, GSH-Px, and T-AOC levels were significantly decreased in aging mice, and that Albicanol treatment significantly increased the serum levels of these antioxidant enzymes. We additionally evaluated the impact of Albicanol treatment on the Keap1/Nrf2/ARE signaling pathway, and found that it was able to decrease Keap1 expression while increasing the expression of Nrf2, thereby activating this signaling pathway, suppressing oxidative damage, and enhancing the expression of downstream target genes including SOD, GSH, GST, HO-1, and NQO1 in this murine aging model system. Albicanol treatment also inhibited the secretion of inflammatory TNF-a and IL-1b. Together, these data indicated that Albicanol can activate Nrf2 pathway-related genes, thereby inhibition of delayed aging by alleviating oxidative stress-induced damage.</description><subject>Aging</subject><subject>Aging (artificial)</subject><subject>Aging (natural)</subject><subject>Animal models</subject><subject>Animal tissues</subject><subject>Antioxidants</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain damage</subject><subject>Brain injury</subject><subject>Cell Biology</subject><subject>D-Galactose</subject><subject>Galactose</subject><subject>Gene expression</subject><subject>Genes</subject><subject>IL-1β</subject><subject>Inflammation</subject><subject>Interleukin 1</subject><subject>Model testing</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Oxidative stress</subject><subject>Senescence</subject><subject>Serum levels</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Tumor necrosis factor-α</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp9kUFv1DAQhS0EokvhD3BAkbhwCYw9WTs5Li2UlSr1UOBqOY69uHKSYier3SP_nClbtlIPvdiW53tvxn6MveXwkQOoT5lzkFUJAkpAQevuGVvwpcJSNoDP2QKQysgbOGGvcr4BIJngL9kJopIcqmrB_qxiG6wZxlisYnTbYCaXi_PywkRjpzG7cj10s3VdsdqEYVOYoSvW_W0at4R9dr_MNozJkLgNMUz74mcwRbs_et1Jrnaho9PWFddTcjkfHc9NbzbuNXvhTczuzf1-yn58_fL97Ft5eXWxPltdlhbVciq9qxupfAud9NILiRLoXqgKva8lNra1UHNlHdqa8wZB2ArpnbUltKo8nrIPB18a_vfs8qT7kK2L0QxunLMWS1iirOlLCX3_CL0Z5zTQdERxVAIUVESJA2XTmHNyXt-m0Ju01xz0XUD6EJCmgPS_gPSORO_uree2d91R8j8RAvAAZCoNG5ceej9h-xcxw5rY</recordid><startdate>20210501</startdate><enddate>20210501</enddate><creator>Chen, Ling Ling</creator><creator>Zhang, Dong Rui</creator><creator>Li, Jie</creator><creator>Wang, He Meng</creator><creator>Song, Chun Hua</creator><creator>Tang, Xun</creator><creator>Guan, Yalin</creator><creator>Chang, Ying</creator><creator>Wang, Wen Fei</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</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>C1K</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>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-6884-5585</orcidid></search><sort><creationdate>20210501</creationdate><title>Albicanol Alleviates D-Galactose-Induced Aging and Improves Behavioral Ability Via by Alleviating Oxidative Stress-Induced Damage</title><author>Chen, Ling Ling ; Zhang, Dong Rui ; Li, Jie ; Wang, He Meng ; Song, Chun Hua ; Tang, Xun ; Guan, Yalin ; Chang, Ying ; Wang, Wen Fei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-fe8967fb0d6f6f263603752743ff8639cbc0817ce3c8119302c433378c63644f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Aging</topic><topic>Aging (artificial)</topic><topic>Aging (natural)</topic><topic>Animal models</topic><topic>Animal tissues</topic><topic>Antioxidants</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain damage</topic><topic>Brain injury</topic><topic>Cell Biology</topic><topic>D-Galactose</topic><topic>Galactose</topic><topic>Gene expression</topic><topic>Genes</topic><topic>IL-1β</topic><topic>Inflammation</topic><topic>Interleukin 1</topic><topic>Model testing</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Oxidative stress</topic><topic>Senescence</topic><topic>Serum levels</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Ling Ling</creatorcontrib><creatorcontrib>Zhang, Dong Rui</creatorcontrib><creatorcontrib>Li, Jie</creatorcontrib><creatorcontrib>Wang, He Meng</creatorcontrib><creatorcontrib>Song, Chun Hua</creatorcontrib><creatorcontrib>Tang, Xun</creatorcontrib><creatorcontrib>Guan, Yalin</creatorcontrib><creatorcontrib>Chang, Ying</creatorcontrib><creatorcontrib>Wang, Wen Fei</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology 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>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>Environmental Sciences and Pollution Management</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>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>MEDLINE - Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Ling Ling</au><au>Zhang, Dong Rui</au><au>Li, Jie</au><au>Wang, He Meng</au><au>Song, Chun Hua</au><au>Tang, Xun</au><au>Guan, Yalin</au><au>Chang, Ying</au><au>Wang, Wen Fei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Albicanol Alleviates D-Galactose-Induced Aging and Improves Behavioral Ability Via by Alleviating Oxidative Stress-Induced Damage</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2021-05-01</date><risdate>2021</risdate><volume>46</volume><issue>5</issue><spage>1058</spage><epage>1067</epage><pages>1058-1067</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Albicanol is a natural terpenoid derived from
Dryopteris fragrans
. Herein, we assessed the ability of Albicanol to protect against oxidative stress-induced senescence. Using a murine model of D-galactose (D-gal)-induced aging, we determined that Albicanol treatment can reverse D-gal-mediated learning impairments and behavioral changes, while also remediating brain tissue damage in treated mice. We found that serum SOD, CAT, GSH-Px, and T-AOC levels were significantly decreased in aging mice, and that Albicanol treatment significantly increased the serum levels of these antioxidant enzymes. We additionally evaluated the impact of Albicanol treatment on the Keap1/Nrf2/ARE signaling pathway, and found that it was able to decrease Keap1 expression while increasing the expression of Nrf2, thereby activating this signaling pathway, suppressing oxidative damage, and enhancing the expression of downstream target genes including SOD, GSH, GST, HO-1, and NQO1 in this murine aging model system. Albicanol treatment also inhibited the secretion of inflammatory TNF-a and IL-1b. Together, these data indicated that Albicanol can activate Nrf2 pathway-related genes, thereby inhibition of delayed aging by alleviating oxidative stress-induced damage.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33761044</pmid><doi>10.1007/s11064-020-03220-x</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-6884-5585</orcidid></addata></record> |
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| subjects | Aging Aging (artificial) Aging (natural) Animal models Animal tissues Antioxidants Biochemistry Biomedical and Life Sciences Biomedicine Brain damage Brain injury Cell Biology D-Galactose Galactose Gene expression Genes IL-1β Inflammation Interleukin 1 Model testing Neurochemistry Neurology Neurosciences Original Paper Oxidative stress Senescence Serum levels Signal transduction Signaling Tumor necrosis factor-α |
| title | Albicanol Alleviates D-Galactose-Induced Aging and Improves Behavioral Ability Via by Alleviating Oxidative Stress-Induced Damage |
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