Protective effect of walnut on d‐galactose‐induced aging mouse model
Objective (s) Accumulating evidence has suggested that oxidative stress and apoptosis are involved in the aging process. d‐galactose (gal) has been reported to cause symptoms of aging in mice, accompanied by liver and brain injuries. Our present work was to study the potential antioxidative and anti...
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Veröffentlicht in: | Food Science & Nutrition 2019-03, Vol.7 (3), p.969-976 |
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creator | Liu, Ji Chen, Dan Wang, Zukun Chen, Chaoyin Ning, Delu Zhao, Shenglan |
description | Objective (s)
Accumulating evidence has suggested that oxidative stress and apoptosis are involved in the aging process. d‐galactose (gal) has been reported to cause symptoms of aging in mice, accompanied by liver and brain injuries. Our present work was to study the potential antioxidative and anti‐apoptotic effects of walnut and to explore how these effects act on mice in a d‐gal‐induced aging model.
Materials and Methods
Aging mice were induced by subcutaneous injection of d‐gal (200 mg kg−1 d−1 for 8 weeks). Walnut samples were simultaneously administered to the d‐gal‐induced aging mice once daily by intragastric gavage. Finally, body weight, organ index, cognitive function, levels of antioxidative enzymes, and liver function were monitored.
Results
The kernel pellicles of walnut could not only improve the learning and memory ability, and the organ index, but also significantly decrease body weight and normalize the levels of activity of antioxidative enzymes in aging mice. Further, the walnut seed coat would protect damages of hippocampus and liver in aging mice.
Highlights
In the current study, we investigated the effects of walnut kernels and walnut seed coats (WSCs) on d‐galactose‐induced aging mice. WSC was firstly found to have beneficial effects on d‐gal‐treated mouse's brain with learning and memory impairment, which probably through the underlying mechanism reduces oxidative damage and limits neuroinflammation. In addition, WSC had a protective effect on liver damage in d‐galactose sensing mice.
Walnut seed coast (WSC) and Walnut seed (WS) could improve the liver and brain damage and the learning and memory impairment in mice induced by d‐gal. |
doi_str_mv | 10.1002/fsn3.907 |
format | Article |
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Accumulating evidence has suggested that oxidative stress and apoptosis are involved in the aging process. d‐galactose (gal) has been reported to cause symptoms of aging in mice, accompanied by liver and brain injuries. Our present work was to study the potential antioxidative and anti‐apoptotic effects of walnut and to explore how these effects act on mice in a d‐gal‐induced aging model.
Materials and Methods
Aging mice were induced by subcutaneous injection of d‐gal (200 mg kg−1 d−1 for 8 weeks). Walnut samples were simultaneously administered to the d‐gal‐induced aging mice once daily by intragastric gavage. Finally, body weight, organ index, cognitive function, levels of antioxidative enzymes, and liver function were monitored.
Results
The kernel pellicles of walnut could not only improve the learning and memory ability, and the organ index, but also significantly decrease body weight and normalize the levels of activity of antioxidative enzymes in aging mice. Further, the walnut seed coat would protect damages of hippocampus and liver in aging mice.
Highlights
In the current study, we investigated the effects of walnut kernels and walnut seed coats (WSCs) on d‐galactose‐induced aging mice. WSC was firstly found to have beneficial effects on d‐gal‐treated mouse's brain with learning and memory impairment, which probably through the underlying mechanism reduces oxidative damage and limits neuroinflammation. In addition, WSC had a protective effect on liver damage in d‐galactose sensing mice.
Walnut seed coast (WSC) and Walnut seed (WS) could improve the liver and brain damage and the learning and memory impairment in mice induced by d‐gal.</description><identifier>ISSN: 2048-7177</identifier><identifier>EISSN: 2048-7177</identifier><identifier>DOI: 10.1002/fsn3.907</identifier><identifier>PMID: 30918639</identifier><language>eng</language><publisher>United States: John Wiley & Sons, Inc</publisher><subject>Aging (artificial) ; Analysis ; Apoptosis ; Body weight ; Brain ; cognitive function ; d‐galactose ; Enzymes ; Galactose ; Head injuries ; Injuries ; Kernels ; Learning ; Liver ; Liver diseases ; Original Research ; Oxidative stress ; walnut ; Walnuts</subject><ispartof>Food Science & Nutrition, 2019-03, Vol.7 (3), p.969-976</ispartof><rights>2019 The Authors. published by Wiley Periodicals, Inc.</rights><rights>COPYRIGHT 2019 John Wiley & Sons, Inc.</rights><rights>2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4727-3cdd2e355b430c9da51a4f05250393ac03be7338201346c93b97f34c50787a7b3</citedby><cites>FETCH-LOGICAL-c4727-3cdd2e355b430c9da51a4f05250393ac03be7338201346c93b97f34c50787a7b3</cites><orcidid>0000-0002-5692-7513</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/PMC6418433/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6418433/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30918639$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Ji</creatorcontrib><creatorcontrib>Chen, Dan</creatorcontrib><creatorcontrib>Wang, Zukun</creatorcontrib><creatorcontrib>Chen, Chaoyin</creatorcontrib><creatorcontrib>Ning, Delu</creatorcontrib><creatorcontrib>Zhao, Shenglan</creatorcontrib><title>Protective effect of walnut on d‐galactose‐induced aging mouse model</title><title>Food Science & Nutrition</title><addtitle>Food Sci Nutr</addtitle><description>Objective (s)
Accumulating evidence has suggested that oxidative stress and apoptosis are involved in the aging process. d‐galactose (gal) has been reported to cause symptoms of aging in mice, accompanied by liver and brain injuries. Our present work was to study the potential antioxidative and anti‐apoptotic effects of walnut and to explore how these effects act on mice in a d‐gal‐induced aging model.
Materials and Methods
Aging mice were induced by subcutaneous injection of d‐gal (200 mg kg−1 d−1 for 8 weeks). Walnut samples were simultaneously administered to the d‐gal‐induced aging mice once daily by intragastric gavage. Finally, body weight, organ index, cognitive function, levels of antioxidative enzymes, and liver function were monitored.
Results
The kernel pellicles of walnut could not only improve the learning and memory ability, and the organ index, but also significantly decrease body weight and normalize the levels of activity of antioxidative enzymes in aging mice. Further, the walnut seed coat would protect damages of hippocampus and liver in aging mice.
Highlights
In the current study, we investigated the effects of walnut kernels and walnut seed coats (WSCs) on d‐galactose‐induced aging mice. WSC was firstly found to have beneficial effects on d‐gal‐treated mouse's brain with learning and memory impairment, which probably through the underlying mechanism reduces oxidative damage and limits neuroinflammation. In addition, WSC had a protective effect on liver damage in d‐galactose sensing mice.
Walnut seed coast (WSC) and Walnut seed (WS) could improve the liver and brain damage and the learning and memory impairment in mice induced by d‐gal.</description><subject>Aging (artificial)</subject><subject>Analysis</subject><subject>Apoptosis</subject><subject>Body weight</subject><subject>Brain</subject><subject>cognitive function</subject><subject>d‐galactose</subject><subject>Enzymes</subject><subject>Galactose</subject><subject>Head injuries</subject><subject>Injuries</subject><subject>Kernels</subject><subject>Learning</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>Original Research</subject><subject>Oxidative stress</subject><subject>walnut</subject><subject>Walnuts</subject><issn>2048-7177</issn><issn>2048-7177</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kdFKHDEUhkOxqNgFn6AM9Mab2SY5mc3kpiCitSBVUK9DJjnZRmYTncwo3vUR-ox9kmbZreiFCSQ_yXf-nPATcsjonFHKv_ocYa6o_ED2ORVtLZmUO6_0HpnlfEfLUIItON8le0AVaxeg9sn51ZBGtGN4xAq9L6pKvnoyfZyKipX7-_vP0vTGjilj0SG6yaKrzDLEZbVKU8ayOuw_kY_e9Bln2_2A3J6d3pyc1xeX33-cHF_UVkgua7DOcYSm6QRQq5xpmBGeNryhoMBYCh1KgJZTBmJhFXRKehC2obKVRnZwQL5tfO-nboXOYhwH0-v7IazM8KyTCfrtTQy_9DI96oVgrQAoBl-2BkN6mDCP-i5NQyw9a84U47KlzZqab6jyedQh-lTMbJkOV8GmiD6U82NJW2iUhLYUHG0K7JByHtC_tMSoXuek1znpklNBP7_-wgv4P5UC1BvgqTzy_K6RPrv-CWvDf5sxnSE</recordid><startdate>201903</startdate><enddate>201903</enddate><creator>Liu, Ji</creator><creator>Chen, Dan</creator><creator>Wang, Zukun</creator><creator>Chen, Chaoyin</creator><creator>Ning, Delu</creator><creator>Zhao, Shenglan</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IAO</scope><scope>3V.</scope><scope>7RV</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0K</scope><scope>M0S</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5692-7513</orcidid></search><sort><creationdate>201903</creationdate><title>Protective effect of walnut on d‐galactose‐induced aging mouse model</title><author>Liu, Ji ; Chen, Dan ; Wang, Zukun ; Chen, Chaoyin ; Ning, Delu ; Zhao, Shenglan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4727-3cdd2e355b430c9da51a4f05250393ac03be7338201346c93b97f34c50787a7b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aging (artificial)</topic><topic>Analysis</topic><topic>Apoptosis</topic><topic>Body weight</topic><topic>Brain</topic><topic>cognitive function</topic><topic>d‐galactose</topic><topic>Enzymes</topic><topic>Galactose</topic><topic>Head injuries</topic><topic>Injuries</topic><topic>Kernels</topic><topic>Learning</topic><topic>Liver</topic><topic>Liver diseases</topic><topic>Original Research</topic><topic>Oxidative stress</topic><topic>walnut</topic><topic>Walnuts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Ji</creatorcontrib><creatorcontrib>Chen, Dan</creatorcontrib><creatorcontrib>Wang, Zukun</creatorcontrib><creatorcontrib>Chen, Chaoyin</creatorcontrib><creatorcontrib>Ning, Delu</creatorcontrib><creatorcontrib>Zhao, Shenglan</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Public Health 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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>Publicly Available Content Database</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>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Food Science & Nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Ji</au><au>Chen, Dan</au><au>Wang, Zukun</au><au>Chen, Chaoyin</au><au>Ning, Delu</au><au>Zhao, Shenglan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective effect of walnut on d‐galactose‐induced aging mouse model</atitle><jtitle>Food Science & Nutrition</jtitle><addtitle>Food Sci Nutr</addtitle><date>2019-03</date><risdate>2019</risdate><volume>7</volume><issue>3</issue><spage>969</spage><epage>976</epage><pages>969-976</pages><issn>2048-7177</issn><eissn>2048-7177</eissn><abstract>Objective (s)
Accumulating evidence has suggested that oxidative stress and apoptosis are involved in the aging process. d‐galactose (gal) has been reported to cause symptoms of aging in mice, accompanied by liver and brain injuries. Our present work was to study the potential antioxidative and anti‐apoptotic effects of walnut and to explore how these effects act on mice in a d‐gal‐induced aging model.
Materials and Methods
Aging mice were induced by subcutaneous injection of d‐gal (200 mg kg−1 d−1 for 8 weeks). Walnut samples were simultaneously administered to the d‐gal‐induced aging mice once daily by intragastric gavage. Finally, body weight, organ index, cognitive function, levels of antioxidative enzymes, and liver function were monitored.
Results
The kernel pellicles of walnut could not only improve the learning and memory ability, and the organ index, but also significantly decrease body weight and normalize the levels of activity of antioxidative enzymes in aging mice. Further, the walnut seed coat would protect damages of hippocampus and liver in aging mice.
Highlights
In the current study, we investigated the effects of walnut kernels and walnut seed coats (WSCs) on d‐galactose‐induced aging mice. WSC was firstly found to have beneficial effects on d‐gal‐treated mouse's brain with learning and memory impairment, which probably through the underlying mechanism reduces oxidative damage and limits neuroinflammation. In addition, WSC had a protective effect on liver damage in d‐galactose sensing mice.
Walnut seed coast (WSC) and Walnut seed (WS) could improve the liver and brain damage and the learning and memory impairment in mice induced by d‐gal.</abstract><cop>United States</cop><pub>John Wiley & Sons, Inc</pub><pmid>30918639</pmid><doi>10.1002/fsn3.907</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-5692-7513</orcidid><oa>free_for_read</oa></addata></record> |
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source | Wiley-Blackwell Open Access Titles; EZB-FREE-00999 freely available EZB journals; Wiley Online Library All Journals; PubMed Central |
subjects | Aging (artificial) Analysis Apoptosis Body weight Brain cognitive function d‐galactose Enzymes Galactose Head injuries Injuries Kernels Learning Liver Liver diseases Original Research Oxidative stress walnut Walnuts |
title | Protective effect of walnut on d‐galactose‐induced aging mouse model |
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