The Dipeptidyl Peptidase-4 Inhibitor Teneligliptin Reduces Aortic Damage from Hypercholesterolaemia in Apolipoprotein E-Deficient Mice
Objective: Hypercholesterolaemia is a well-established risk factor for blood vessel damage, which can lead to cardiovascular diseases. An abundance of clinical data show that dipeptidyl peptidase-4 inhibitors protect against aortic damage in patients with diabetes. The goal of this study was to inve...
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| Veröffentlicht in: | Biomedicine hub 2017-05, Vol.2 (2), p.1-9 |
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| creator | Zhang, Ying Wang, Nan Zhu, Liyue Liu, Yingshu Pei, Zuowei Wang, Guan Luo, Lin Liu, Hongyang |
| description | Objective: Hypercholesterolaemia is a well-established risk factor for blood vessel damage, which can lead to cardiovascular diseases. An abundance of clinical data show that dipeptidyl peptidase-4 inhibitors protect against aortic damage in patients with diabetes. The goal of this study was to investigate the possible protective effects of teneligliptin against aortic damage in apolipoprotein E knockout (ApoE -/- ) mice. Methods: Eight-week-old male ApoE -/- mice were randomly divided into 3 groups: a control group fed a normal diet, a high-cholesterol diet (HD group), and an HD diet mixed with teneligliptin (HD + Tene group), and all the groups were fed with the different treatments for 6 weeks. Results and Conclusion: The metabolic characteristics of total cholesterol, low-density lipoprotein-cholesterol, and high-sensitivity C-reactive protein were lower in ApoE -/- HD + Tene mice than in ApoE -/- HD mice. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) gene and protein expression were lower in the aortic tissue of ApoE -/- HD + Tene mice than in ApoE -/- HD mice. IL-6 and TNF-α gene expression were lower in ApoE -/- HD + Tene mice than in ApoE -/- HD mice. These results indicate that teneligliptin may provide a potential therapeutic target for the aortic damage from hypercholesterolaemia. |
| doi_str_mv | 10.1159/000473869 |
| format | Article |
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An abundance of clinical data show that dipeptidyl peptidase-4 inhibitors protect against aortic damage in patients with diabetes. The goal of this study was to investigate the possible protective effects of teneligliptin against aortic damage in apolipoprotein E knockout (ApoE -/- ) mice. Methods: Eight-week-old male ApoE -/- mice were randomly divided into 3 groups: a control group fed a normal diet, a high-cholesterol diet (HD group), and an HD diet mixed with teneligliptin (HD + Tene group), and all the groups were fed with the different treatments for 6 weeks. Results and Conclusion: The metabolic characteristics of total cholesterol, low-density lipoprotein-cholesterol, and high-sensitivity C-reactive protein were lower in ApoE -/- HD + Tene mice than in ApoE -/- HD mice. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) gene and protein expression were lower in the aortic tissue of ApoE -/- HD + Tene mice than in ApoE -/- HD mice. IL-6 and TNF-α gene expression were lower in ApoE -/- HD + Tene mice than in ApoE -/- HD mice. These results indicate that teneligliptin may provide a potential therapeutic target for the aortic damage from hypercholesterolaemia.</description><identifier>ISSN: 2296-6870</identifier><identifier>ISSN: 2296-6862</identifier><identifier>EISSN: 2296-6870</identifier><identifier>DOI: 10.1159/000473869</identifier><identifier>PMID: 31988912</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Apolipoproteins ; Atherosclerosis ; Cardiovascular disease ; Cholesterol ; Collagen ; Coronary vessels ; Diet ; Gene expression ; Glucose ; Kinases ; Laboratory animals ; Lipids ; Lipoproteins ; Metabolism ; Polyclonal antibodies ; Proteins ; Research Article ; Rodents ; Signal transduction ; Software ; Statistical analysis</subject><ispartof>Biomedicine hub, 2017-05, Vol.2 (2), p.1-9</ispartof><rights>2017 The Author(s) Published by S. Karger AG, Basel</rights><rights>Copyright © 2017 by S. Karger AG, Basel.</rights><rights>Copyright © 2017 by S. Karger AG, Basel 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2979-ff86af332772db3ed856bb62300fba7fc8a4642cc6f589cd7e1a6b8facee448b3</citedby><cites>FETCH-LOGICAL-c2979-ff86af332772db3ed856bb62300fba7fc8a4642cc6f589cd7e1a6b8facee448b3</cites><orcidid>0000-0002-2213-8719</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/PMC6945959/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6945959/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27635,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31988912$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Ying</creatorcontrib><creatorcontrib>Wang, Nan</creatorcontrib><creatorcontrib>Zhu, Liyue</creatorcontrib><creatorcontrib>Liu, Yingshu</creatorcontrib><creatorcontrib>Pei, Zuowei</creatorcontrib><creatorcontrib>Wang, Guan</creatorcontrib><creatorcontrib>Luo, Lin</creatorcontrib><creatorcontrib>Liu, Hongyang</creatorcontrib><title>The Dipeptidyl Peptidase-4 Inhibitor Teneligliptin Reduces Aortic Damage from Hypercholesterolaemia in Apolipoprotein E-Deficient Mice</title><title>Biomedicine hub</title><addtitle>Biomed Hub</addtitle><description>Objective: Hypercholesterolaemia is a well-established risk factor for blood vessel damage, which can lead to cardiovascular diseases. An abundance of clinical data show that dipeptidyl peptidase-4 inhibitors protect against aortic damage in patients with diabetes. The goal of this study was to investigate the possible protective effects of teneligliptin against aortic damage in apolipoprotein E knockout (ApoE -/- ) mice. Methods: Eight-week-old male ApoE -/- mice were randomly divided into 3 groups: a control group fed a normal diet, a high-cholesterol diet (HD group), and an HD diet mixed with teneligliptin (HD + Tene group), and all the groups were fed with the different treatments for 6 weeks. Results and Conclusion: The metabolic characteristics of total cholesterol, low-density lipoprotein-cholesterol, and high-sensitivity C-reactive protein were lower in ApoE -/- HD + Tene mice than in ApoE -/- HD mice. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) gene and protein expression were lower in the aortic tissue of ApoE -/- HD + Tene mice than in ApoE -/- HD mice. IL-6 and TNF-α gene expression were lower in ApoE -/- HD + Tene mice than in ApoE -/- HD mice. These results indicate that teneligliptin may provide a potential therapeutic target for the aortic damage from hypercholesterolaemia.</description><subject>Apolipoproteins</subject><subject>Atherosclerosis</subject><subject>Cardiovascular disease</subject><subject>Cholesterol</subject><subject>Collagen</subject><subject>Coronary vessels</subject><subject>Diet</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Lipids</subject><subject>Lipoproteins</subject><subject>Metabolism</subject><subject>Polyclonal antibodies</subject><subject>Proteins</subject><subject>Research Article</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Software</subject><subject>Statistical analysis</subject><issn>2296-6870</issn><issn>2296-6862</issn><issn>2296-6870</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkU9v1DAQxS0EolXpgTtClrjAIeA_iWNfkJZuYSu1AqHlbDnOeNcliVM7QdovwOfGsMtSECePNb95b0YPoaeUvKa0Um8IIWXNpVAP0CljShRC1uThvfoEnad0mzEqWU0Ff4xOOFVSKspO0ff1FvDSjzBOvt11-NOvwiQoSnw1bH3jpxDxGgbo_KbzuTngz9DOFhJehDh5i5emNxvALoYer3YjRLsNHaQJYugM9N7gPLMYQ54OYwwT5O9lsQTnrYdhwjfewhP0yJkuwfnhPUNf3l-uL1bF9ccPVxeL68IyVavCOSmM45zVNWsbDq2sRNMIxglxjamdlaYUJbNWuEoq29ZAjWikMxagLGXDz9Dbve44Nz20NvtH0-kx-t7EnQ7G6787g9_qTfimhSorVaks8PIgEMPdnK_UvU8Wus4MEOakGS_rilImZUZf_IPehjkO-TxNlSKVoJyUmXq1p2wMKUVwx2Uo0T8D1seAM_v8_vZH8necfyy_mriBeATe3az2EnpsXaae_Zc6uPwAwtq4PQ</recordid><startdate>20170520</startdate><enddate>20170520</enddate><creator>Zhang, Ying</creator><creator>Wang, Nan</creator><creator>Zhu, Liyue</creator><creator>Liu, Yingshu</creator><creator>Pei, Zuowei</creator><creator>Wang, Guan</creator><creator>Luo, Lin</creator><creator>Liu, Hongyang</creator><general>S. 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Liu, Yingshu ; Pei, Zuowei ; Wang, Guan ; Luo, Lin ; Liu, Hongyang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2979-ff86af332772db3ed856bb62300fba7fc8a4642cc6f589cd7e1a6b8facee448b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Apolipoproteins</topic><topic>Atherosclerosis</topic><topic>Cardiovascular disease</topic><topic>Cholesterol</topic><topic>Collagen</topic><topic>Coronary vessels</topic><topic>Diet</topic><topic>Gene expression</topic><topic>Glucose</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Lipids</topic><topic>Lipoproteins</topic><topic>Metabolism</topic><topic>Polyclonal antibodies</topic><topic>Proteins</topic><topic>Research Article</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Software</topic><topic>Statistical analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Ying</creatorcontrib><creatorcontrib>Wang, Nan</creatorcontrib><creatorcontrib>Zhu, Liyue</creatorcontrib><creatorcontrib>Liu, Yingshu</creatorcontrib><creatorcontrib>Pei, Zuowei</creatorcontrib><creatorcontrib>Wang, Guan</creatorcontrib><creatorcontrib>Luo, Lin</creatorcontrib><creatorcontrib>Liu, Hongyang</creatorcontrib><collection>Karger Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>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>AIDS and Cancer Research Abstracts</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>Biological Science 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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Biomedicine hub</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Ying</au><au>Wang, Nan</au><au>Zhu, Liyue</au><au>Liu, Yingshu</au><au>Pei, Zuowei</au><au>Wang, Guan</au><au>Luo, Lin</au><au>Liu, Hongyang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Dipeptidyl Peptidase-4 Inhibitor Teneligliptin Reduces Aortic Damage from Hypercholesterolaemia in Apolipoprotein E-Deficient Mice</atitle><jtitle>Biomedicine hub</jtitle><addtitle>Biomed Hub</addtitle><date>2017-05-20</date><risdate>2017</risdate><volume>2</volume><issue>2</issue><spage>1</spage><epage>9</epage><pages>1-9</pages><issn>2296-6870</issn><issn>2296-6862</issn><eissn>2296-6870</eissn><abstract>Objective: Hypercholesterolaemia is a well-established risk factor for blood vessel damage, which can lead to cardiovascular diseases. An abundance of clinical data show that dipeptidyl peptidase-4 inhibitors protect against aortic damage in patients with diabetes. The goal of this study was to investigate the possible protective effects of teneligliptin against aortic damage in apolipoprotein E knockout (ApoE -/- ) mice. Methods: Eight-week-old male ApoE -/- mice were randomly divided into 3 groups: a control group fed a normal diet, a high-cholesterol diet (HD group), and an HD diet mixed with teneligliptin (HD + Tene group), and all the groups were fed with the different treatments for 6 weeks. Results and Conclusion: The metabolic characteristics of total cholesterol, low-density lipoprotein-cholesterol, and high-sensitivity C-reactive protein were lower in ApoE -/- HD + Tene mice than in ApoE -/- HD mice. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) gene and protein expression were lower in the aortic tissue of ApoE -/- HD + Tene mice than in ApoE -/- HD mice. IL-6 and TNF-α gene expression were lower in ApoE -/- HD + Tene mice than in ApoE -/- HD mice. These results indicate that teneligliptin may provide a potential therapeutic target for the aortic damage from hypercholesterolaemia.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>31988912</pmid><doi>10.1159/000473869</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-2213-8719</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Apolipoproteins Atherosclerosis Cardiovascular disease Cholesterol Collagen Coronary vessels Diet Gene expression Glucose Kinases Laboratory animals Lipids Lipoproteins Metabolism Polyclonal antibodies Proteins Research Article Rodents Signal transduction Software Statistical analysis |
| title | The Dipeptidyl Peptidase-4 Inhibitor Teneligliptin Reduces Aortic Damage from Hypercholesterolaemia in Apolipoprotein E-Deficient Mice |
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