Ginsenoside Rg1 Ameliorates Behavioral Abnormalities and Modulates the Hippocampal Proteomic Change in Triple Transgenic Mice of Alzheimer’s Disease
Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, so far, there are no effective measures to prevent and cure this deadly condition. Ginsenoside Rg1 (Rg1) was shown to improve behavioral abnormalities in AD; however, the potential mechanisms remain unclear. In this study...
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| creator | Yang, Xifei Liu, Jianjun Huang, Xinfeng Yang, Ying Zhang, Zai Jun Li, Honglian Xia, Junxia Nie, Lulin He, Zhendan |
| description | Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, so far, there are no effective measures to prevent and cure this deadly condition. Ginsenoside Rg1 (Rg1) was shown to improve behavioral abnormalities in AD; however, the potential mechanisms remain unclear. In this study, we pretreated 7-month-old 3xTg-AD mice for 6 weeks with Rg1 and evaluated the effects of Rg1 on the behaviors and the protein expression of hippocampal tissues. The behavioral tests showed that Rg1 could improve the memory impairment and ameliorate the depression-like behaviors of 3xTg-AD mice. Proteomic results revealed a total of 28 differentially expressed hippocampal proteins between Rg1-treated and nontreated 3xTg-AD mice. Among these proteins, complexin-2 (CPLX2), synapsin-2 (SYN2), and synaptosomal-associated protein 25 (SNP25) were significantly downregulated in the hippocampus of 3xTg-AD mice compared with the WT mice, and the treatment of Rg1 modulated the expression of CPLX2 and SNP25 in the hippocampus of 3xTg-AD mice. The expression of CPLX2, SYN2, and SNP25 was further validated by Western blot analysis. Taken together, we concluded that Rg1 could be a potential candidate drug to improve the behavioral deficits in AD via modulating the expression of the proteins (i.e., CPLX2, SYN2, and SNP25). |
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Ginsenoside Rg1 (Rg1) was shown to improve behavioral abnormalities in AD; however, the potential mechanisms remain unclear. In this study, we pretreated 7-month-old 3xTg-AD mice for 6 weeks with Rg1 and evaluated the effects of Rg1 on the behaviors and the protein expression of hippocampal tissues. The behavioral tests showed that Rg1 could improve the memory impairment and ameliorate the depression-like behaviors of 3xTg-AD mice. Proteomic results revealed a total of 28 differentially expressed hippocampal proteins between Rg1-treated and nontreated 3xTg-AD mice. Among these proteins, complexin-2 (CPLX2), synapsin-2 (SYN2), and synaptosomal-associated protein 25 (SNP25) were significantly downregulated in the hippocampus of 3xTg-AD mice compared with the WT mice, and the treatment of Rg1 modulated the expression of CPLX2 and SNP25 in the hippocampus of 3xTg-AD mice. The expression of CPLX2, SYN2, and SNP25 was further validated by Western blot analysis. Taken together, we concluded that Rg1 could be a potential candidate drug to improve the behavioral deficits in AD via modulating the expression of the proteins (i.e., CPLX2, SYN2, and SNP25).</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2017/6473506</identifier><identifier>PMID: 29204248</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Advertising executives ; Aging ; Alzheimer's disease ; Anxiety ; Behavior ; Brain research ; Cognitive ability ; Dementia ; Depression, Mental ; Disease control ; Genetic engineering ; Laboratories ; Memory ; Mental depression ; Neurobiology ; Neurodegeneration ; Neurosciences ; Pharmacy ; Proteins ; Rodents ; Transgenic animals</subject><ispartof>Oxidative medicine and cellular longevity, 2017-01, Vol.2017 (2017), p.1-17</ispartof><rights>Copyright © 2017 Lulin Nie et al.</rights><rights>COPYRIGHT 2017 John Wiley & Sons, Inc.</rights><rights>Copyright © 2017 Lulin Nie et al.; This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2017 Lulin Nie et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-c1708edf86d817df3d9d72afc43d708350c65b9f9bad942c7069821fd6910ab93</citedby><cites>FETCH-LOGICAL-c499t-c1708edf86d817df3d9d72afc43d708350c65b9f9bad942c7069821fd6910ab93</cites><orcidid>0000-0002-9000-7016</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/PMC5674513/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5674513/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29204248$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Zolezzi, Juan M.</contributor><creatorcontrib>Yang, Xifei</creatorcontrib><creatorcontrib>Liu, Jianjun</creatorcontrib><creatorcontrib>Huang, Xinfeng</creatorcontrib><creatorcontrib>Yang, Ying</creatorcontrib><creatorcontrib>Zhang, Zai Jun</creatorcontrib><creatorcontrib>Li, Honglian</creatorcontrib><creatorcontrib>Xia, Junxia</creatorcontrib><creatorcontrib>Nie, Lulin</creatorcontrib><creatorcontrib>He, Zhendan</creatorcontrib><title>Ginsenoside Rg1 Ameliorates Behavioral Abnormalities and Modulates the Hippocampal Proteomic Change in Triple Transgenic Mice of Alzheimer’s Disease</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, so far, there are no effective measures to prevent and cure this deadly condition. Ginsenoside Rg1 (Rg1) was shown to improve behavioral abnormalities in AD; however, the potential mechanisms remain unclear. In this study, we pretreated 7-month-old 3xTg-AD mice for 6 weeks with Rg1 and evaluated the effects of Rg1 on the behaviors and the protein expression of hippocampal tissues. The behavioral tests showed that Rg1 could improve the memory impairment and ameliorate the depression-like behaviors of 3xTg-AD mice. Proteomic results revealed a total of 28 differentially expressed hippocampal proteins between Rg1-treated and nontreated 3xTg-AD mice. Among these proteins, complexin-2 (CPLX2), synapsin-2 (SYN2), and synaptosomal-associated protein 25 (SNP25) were significantly downregulated in the hippocampus of 3xTg-AD mice compared with the WT mice, and the treatment of Rg1 modulated the expression of CPLX2 and SNP25 in the hippocampus of 3xTg-AD mice. The expression of CPLX2, SYN2, and SNP25 was further validated by Western blot analysis. Taken together, we concluded that Rg1 could be a potential candidate drug to improve the behavioral deficits in AD via modulating the expression of the proteins (i.e., CPLX2, SYN2, and SNP25).</description><subject>Advertising executives</subject><subject>Aging</subject><subject>Alzheimer's disease</subject><subject>Anxiety</subject><subject>Behavior</subject><subject>Brain research</subject><subject>Cognitive ability</subject><subject>Dementia</subject><subject>Depression, Mental</subject><subject>Disease control</subject><subject>Genetic engineering</subject><subject>Laboratories</subject><subject>Memory</subject><subject>Mental depression</subject><subject>Neurobiology</subject><subject>Neurodegeneration</subject><subject>Neurosciences</subject><subject>Pharmacy</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Transgenic animals</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>RHX</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>eNqNksFu1DAQhiMEoqVw44wscUGCpbZjJ_EFKSzQIrUCoXK2HHuycZXYqZ0UwYmnQOL1eBIcdtkCJ05j6__0e2b8Z9lDgp8TwvkxxaQ8LliZc1zcyg6JYHSFhWC392eMD7J7MV5iXOSUkbvZARUUM8qqw-zbiXURnI_WAPqwIageoLc-qAkiegmdul4uPaob58OgejvZJChn0Lk3c_8LmzpAp3YcvVbDmNj3wU_gB6vRulNuA8g6dBHs2EMqysUNuKSdWw3It6juv3RgBwg_vn6P6JWNoCLcz-60qo_wYFePso9vXl-sT1dn707eruuzlWZCTCtNSlyBaavCVKQ0bW6EKalqNctNUtJKdMEb0YpGmbQLXeJCVJS0phAEq0bkR9mLre84NwMYDW5K08ox2EGFz9IrK_9WnO3kxl9LXpSMkzwZPNkZBH81Q5zkYKOGvlcO_BwlEWWOKaF5mdDH_6CXfg4ujZeogrCcViW5oTaqB2ld69O7ejGVNee8Sr9cLX0_21I6-BgDtPuWCZZLLOQSC7mLRcIf_TnmHv6dgwQ83QKddUZ9sv9pB4mBVt3QRPDF7ie-jMud</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Yang, Xifei</creator><creator>Liu, Jianjun</creator><creator>Huang, Xinfeng</creator><creator>Yang, Ying</creator><creator>Zhang, Zai Jun</creator><creator>Li, Honglian</creator><creator>Xia, Junxia</creator><creator>Nie, Lulin</creator><creator>He, Zhendan</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9000-7016</orcidid></search><sort><creationdate>20170101</creationdate><title>Ginsenoside Rg1 Ameliorates Behavioral Abnormalities and Modulates the Hippocampal Proteomic Change in Triple Transgenic Mice of Alzheimer’s Disease</title><author>Yang, Xifei ; 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Ginsenoside Rg1 (Rg1) was shown to improve behavioral abnormalities in AD; however, the potential mechanisms remain unclear. In this study, we pretreated 7-month-old 3xTg-AD mice for 6 weeks with Rg1 and evaluated the effects of Rg1 on the behaviors and the protein expression of hippocampal tissues. The behavioral tests showed that Rg1 could improve the memory impairment and ameliorate the depression-like behaviors of 3xTg-AD mice. Proteomic results revealed a total of 28 differentially expressed hippocampal proteins between Rg1-treated and nontreated 3xTg-AD mice. Among these proteins, complexin-2 (CPLX2), synapsin-2 (SYN2), and synaptosomal-associated protein 25 (SNP25) were significantly downregulated in the hippocampus of 3xTg-AD mice compared with the WT mice, and the treatment of Rg1 modulated the expression of CPLX2 and SNP25 in the hippocampus of 3xTg-AD mice. The expression of CPLX2, SYN2, and SNP25 was further validated by Western blot analysis. Taken together, we concluded that Rg1 could be a potential candidate drug to improve the behavioral deficits in AD via modulating the expression of the proteins (i.e., CPLX2, SYN2, and SNP25).</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>29204248</pmid><doi>10.1155/2017/6473506</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-9000-7016</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Wiley-Blackwell Open Access Titles; PubMed Central; Alma/SFX Local Collection |
| subjects | Advertising executives Aging Alzheimer's disease Anxiety Behavior Brain research Cognitive ability Dementia Depression, Mental Disease control Genetic engineering Laboratories Memory Mental depression Neurobiology Neurodegeneration Neurosciences Pharmacy Proteins Rodents Transgenic animals |
| title | Ginsenoside Rg1 Ameliorates Behavioral Abnormalities and Modulates the Hippocampal Proteomic Change in Triple Transgenic Mice of Alzheimer’s Disease |
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