Tenuifolin ameliorates the sleep deprivation‐induced cognitive deficits
Tenuifolin (TEN), a natural neuroprotective compound obtained from the Polygala tenuifolia Willd plant, has improved cognitive symptoms. However, the impact of TEN on memory impairments caused by sleep deprivation (SD) is unclear. Accordingly, the objective of this study was to investigate the mecha...
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| Veröffentlicht in: | Phytotherapy research 2023-02, Vol.37 (2), p.464-476 |
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| creator | Jiang, Ning Zhang, Yiwen Yao, Caihong Liu, Yupei Chen, Yuzhen Chen, Fang Wang, Yan Choudhary, Muhammad Iqbal Liu, Xinmin |
| description | Tenuifolin (TEN), a natural neuroprotective compound obtained from the Polygala tenuifolia Willd plant, has improved cognitive symptoms. However, the impact of TEN on memory impairments caused by sleep deprivation (SD) is unclear. Accordingly, the objective of this study was to investigate the mechanisms behind the preventative benefits of TEN on cognitive impairment caused by SD. TEN (10 and 20 mg/kg) and Huperzine A (0.1 mg/kg) were given to mice through oral gavage for 28 days during the SD process. The results indicate that TEN administrations improve short‐ and long‐term memory impairments caused by SD in the Y‐maze, object identification, and step‐through tests. Moreover, TEN stimulated the generation of anti‐inflammatory cytokines (interleukin‐10), lowered the production of pro‐inflammatory cytokines (interleukin‐1β, interleukin‐6, and interleukin‐18), and activated microglia, improving antioxidant status in the hippocampus. TEN treatments significantly boosted the expression of nuclear factor erythroid 2‐related factor 2 and heme oxygenase‐1 while considerably decreasing the expression of NOD‐like receptor thermal protein domain associated protein 3 and caspase‐1 p20. Additionally, TEN restored the downregulation of the brain‐derived neurotrophic factor signaling cascade and the impaired hippocampal neurogenesis induced by SD. When considered collectively, our data suggest that TEN is a potentially effective neuroprotective agent for cognition dysfunction. |
| doi_str_mv | 10.1002/ptr.7627 |
| format | Article |
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However, the impact of TEN on memory impairments caused by sleep deprivation (SD) is unclear. Accordingly, the objective of this study was to investigate the mechanisms behind the preventative benefits of TEN on cognitive impairment caused by SD. TEN (10 and 20 mg/kg) and Huperzine A (0.1 mg/kg) were given to mice through oral gavage for 28 days during the SD process. The results indicate that TEN administrations improve short‐ and long‐term memory impairments caused by SD in the Y‐maze, object identification, and step‐through tests. Moreover, TEN stimulated the generation of anti‐inflammatory cytokines (interleukin‐10), lowered the production of pro‐inflammatory cytokines (interleukin‐1β, interleukin‐6, and interleukin‐18), and activated microglia, improving antioxidant status in the hippocampus. TEN treatments significantly boosted the expression of nuclear factor erythroid 2‐related factor 2 and heme oxygenase‐1 while considerably decreasing the expression of NOD‐like receptor thermal protein domain associated protein 3 and caspase‐1 p20. Additionally, TEN restored the downregulation of the brain‐derived neurotrophic factor signaling cascade and the impaired hippocampal neurogenesis induced by SD. When considered collectively, our data suggest that TEN is a potentially effective neuroprotective agent for cognition dysfunction.</description><identifier>ISSN: 0951-418X</identifier><identifier>EISSN: 1099-1573</identifier><identifier>DOI: 10.1002/ptr.7627</identifier><identifier>PMID: 36608695</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Animals ; Caspase ; Cognition ; cognitive ; Cognitive ability ; Cognitive Dysfunction - drug therapy ; Cytokines ; Cytokines - metabolism ; Heme ; Hippocampus ; Huperzine A ; Inflammation ; inflammatory response ; Interleukin 6 ; Maze Learning ; Memory ; Mice ; Microglia ; Neurogenesis ; Neuroprotection ; Neurotrophic factors ; Oxidative stress ; Oxygenase ; Proteins ; Sleep deprivation ; Sleep Deprivation - complications ; Sleep Deprivation - drug therapy ; tenuifolin</subject><ispartof>Phytotherapy research, 2023-02, Vol.37 (2), p.464-476</ispartof><rights>2023 John Wiley & Sons Ltd.</rights><rights>2023 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3497-8551c9619a6f805748885fbf6d77e9d0e96e0ffbc3360f722561cf4ebb6fb0e3</citedby><cites>FETCH-LOGICAL-c3497-8551c9619a6f805748885fbf6d77e9d0e96e0ffbc3360f722561cf4ebb6fb0e3</cites><orcidid>0000-0001-6452-4645 ; 0000-0001-5356-3585</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%2Fptr.7627$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fptr.7627$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27922,27923,45572,45573</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36608695$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Ning</creatorcontrib><creatorcontrib>Zhang, Yiwen</creatorcontrib><creatorcontrib>Yao, Caihong</creatorcontrib><creatorcontrib>Liu, Yupei</creatorcontrib><creatorcontrib>Chen, Yuzhen</creatorcontrib><creatorcontrib>Chen, Fang</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Choudhary, Muhammad Iqbal</creatorcontrib><creatorcontrib>Liu, Xinmin</creatorcontrib><title>Tenuifolin ameliorates the sleep deprivation‐induced cognitive deficits</title><title>Phytotherapy research</title><addtitle>Phytother Res</addtitle><description>Tenuifolin (TEN), a natural neuroprotective compound obtained from the Polygala tenuifolia Willd plant, has improved cognitive symptoms. However, the impact of TEN on memory impairments caused by sleep deprivation (SD) is unclear. Accordingly, the objective of this study was to investigate the mechanisms behind the preventative benefits of TEN on cognitive impairment caused by SD. TEN (10 and 20 mg/kg) and Huperzine A (0.1 mg/kg) were given to mice through oral gavage for 28 days during the SD process. The results indicate that TEN administrations improve short‐ and long‐term memory impairments caused by SD in the Y‐maze, object identification, and step‐through tests. Moreover, TEN stimulated the generation of anti‐inflammatory cytokines (interleukin‐10), lowered the production of pro‐inflammatory cytokines (interleukin‐1β, interleukin‐6, and interleukin‐18), and activated microglia, improving antioxidant status in the hippocampus. TEN treatments significantly boosted the expression of nuclear factor erythroid 2‐related factor 2 and heme oxygenase‐1 while considerably decreasing the expression of NOD‐like receptor thermal protein domain associated protein 3 and caspase‐1 p20. Additionally, TEN restored the downregulation of the brain‐derived neurotrophic factor signaling cascade and the impaired hippocampal neurogenesis induced by SD. When considered collectively, our data suggest that TEN is a potentially effective neuroprotective agent for cognition dysfunction.</description><subject>Animals</subject><subject>Caspase</subject><subject>Cognition</subject><subject>cognitive</subject><subject>Cognitive ability</subject><subject>Cognitive Dysfunction - drug therapy</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Heme</subject><subject>Hippocampus</subject><subject>Huperzine A</subject><subject>Inflammation</subject><subject>inflammatory response</subject><subject>Interleukin 6</subject><subject>Maze Learning</subject><subject>Memory</subject><subject>Mice</subject><subject>Microglia</subject><subject>Neurogenesis</subject><subject>Neuroprotection</subject><subject>Neurotrophic factors</subject><subject>Oxidative stress</subject><subject>Oxygenase</subject><subject>Proteins</subject><subject>Sleep deprivation</subject><subject>Sleep Deprivation - complications</subject><subject>Sleep Deprivation - drug therapy</subject><subject>tenuifolin</subject><issn>0951-418X</issn><issn>1099-1573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kL1OwzAQgC0EoqUg8QQoEgtLyjmO7XhEiJ9KlUAoA5uVOGdwlSYhToq68Qg8I09CSgsb0w336TvdR8gphSkFiC6brp1KEck9MqagVEi5ZPtkDIrTMKbJ84gceb8AABVBfEhGTAhIhOJjMkux6p2tS1cF2RJLV7dZhz7oXjHwJWITFNi0bpV1rq6-Pj5dVfQGi8DUL5Xr3AqHvXXGdf6YHNis9HiymxOS3t6k1_fh_OFudn01Dw2LlQwTzqlRgqpM2AS4jJMk4Ta3opASVQGoBIK1uWFMgJVRxAU1NsY8FzYHZBNyvtU2bf3Wo-_0ou7barioIyklsAiYHKiLLWXa2vsWrR6eWGbtWlPQm2R6SKY3yQb0bCfs8yUWf-BvowEIt8C7K3H9r0g_pk8_wm-Acnbu</recordid><startdate>202302</startdate><enddate>202302</enddate><creator>Jiang, Ning</creator><creator>Zhang, Yiwen</creator><creator>Yao, Caihong</creator><creator>Liu, Yupei</creator><creator>Chen, Yuzhen</creator><creator>Chen, Fang</creator><creator>Wang, Yan</creator><creator>Choudhary, Muhammad Iqbal</creator><creator>Liu, Xinmin</creator><general>John Wiley & Sons, Ltd</general><general>Wiley Subscription Services, Inc</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>7QO</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><orcidid>https://orcid.org/0000-0001-6452-4645</orcidid><orcidid>https://orcid.org/0000-0001-5356-3585</orcidid></search><sort><creationdate>202302</creationdate><title>Tenuifolin ameliorates the sleep deprivation‐induced cognitive deficits</title><author>Jiang, Ning ; Zhang, Yiwen ; Yao, Caihong ; Liu, Yupei ; Chen, Yuzhen ; Chen, Fang ; Wang, Yan ; Choudhary, Muhammad Iqbal ; Liu, Xinmin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3497-8551c9619a6f805748885fbf6d77e9d0e96e0ffbc3360f722561cf4ebb6fb0e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Caspase</topic><topic>Cognition</topic><topic>cognitive</topic><topic>Cognitive ability</topic><topic>Cognitive Dysfunction - drug therapy</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Heme</topic><topic>Hippocampus</topic><topic>Huperzine A</topic><topic>Inflammation</topic><topic>inflammatory response</topic><topic>Interleukin 6</topic><topic>Maze Learning</topic><topic>Memory</topic><topic>Mice</topic><topic>Microglia</topic><topic>Neurogenesis</topic><topic>Neuroprotection</topic><topic>Neurotrophic factors</topic><topic>Oxidative stress</topic><topic>Oxygenase</topic><topic>Proteins</topic><topic>Sleep deprivation</topic><topic>Sleep Deprivation - complications</topic><topic>Sleep Deprivation - drug therapy</topic><topic>tenuifolin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Ning</creatorcontrib><creatorcontrib>Zhang, Yiwen</creatorcontrib><creatorcontrib>Yao, Caihong</creatorcontrib><creatorcontrib>Liu, Yupei</creatorcontrib><creatorcontrib>Chen, Yuzhen</creatorcontrib><creatorcontrib>Chen, Fang</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Choudhary, Muhammad Iqbal</creatorcontrib><creatorcontrib>Liu, Xinmin</creatorcontrib><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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Phytotherapy research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Ning</au><au>Zhang, Yiwen</au><au>Yao, Caihong</au><au>Liu, Yupei</au><au>Chen, Yuzhen</au><au>Chen, Fang</au><au>Wang, Yan</au><au>Choudhary, Muhammad Iqbal</au><au>Liu, Xinmin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tenuifolin ameliorates the sleep deprivation‐induced cognitive deficits</atitle><jtitle>Phytotherapy research</jtitle><addtitle>Phytother Res</addtitle><date>2023-02</date><risdate>2023</risdate><volume>37</volume><issue>2</issue><spage>464</spage><epage>476</epage><pages>464-476</pages><issn>0951-418X</issn><eissn>1099-1573</eissn><abstract>Tenuifolin (TEN), a natural neuroprotective compound obtained from the Polygala tenuifolia Willd plant, has improved cognitive symptoms. However, the impact of TEN on memory impairments caused by sleep deprivation (SD) is unclear. Accordingly, the objective of this study was to investigate the mechanisms behind the preventative benefits of TEN on cognitive impairment caused by SD. TEN (10 and 20 mg/kg) and Huperzine A (0.1 mg/kg) were given to mice through oral gavage for 28 days during the SD process. The results indicate that TEN administrations improve short‐ and long‐term memory impairments caused by SD in the Y‐maze, object identification, and step‐through tests. Moreover, TEN stimulated the generation of anti‐inflammatory cytokines (interleukin‐10), lowered the production of pro‐inflammatory cytokines (interleukin‐1β, interleukin‐6, and interleukin‐18), and activated microglia, improving antioxidant status in the hippocampus. TEN treatments significantly boosted the expression of nuclear factor erythroid 2‐related factor 2 and heme oxygenase‐1 while considerably decreasing the expression of NOD‐like receptor thermal protein domain associated protein 3 and caspase‐1 p20. Additionally, TEN restored the downregulation of the brain‐derived neurotrophic factor signaling cascade and the impaired hippocampal neurogenesis induced by SD. When considered collectively, our data suggest that TEN is a potentially effective neuroprotective agent for cognition dysfunction.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>36608695</pmid><doi>10.1002/ptr.7627</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-6452-4645</orcidid><orcidid>https://orcid.org/0000-0001-5356-3585</orcidid></addata></record> |
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| subjects | Animals Caspase Cognition cognitive Cognitive ability Cognitive Dysfunction - drug therapy Cytokines Cytokines - metabolism Heme Hippocampus Huperzine A Inflammation inflammatory response Interleukin 6 Maze Learning Memory Mice Microglia Neurogenesis Neuroprotection Neurotrophic factors Oxidative stress Oxygenase Proteins Sleep deprivation Sleep Deprivation - complications Sleep Deprivation - drug therapy tenuifolin |
| title | Tenuifolin ameliorates the sleep deprivation‐induced cognitive deficits |
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