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Probucol prevents the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbit, an animal model for familial hypercholesterolemia
In this study, we questioned whether in vivo probucol could prevent the progression of atherosclerosis in homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits, an animal model for familial hypercholesterolemia. At 2 months of age, eight WHHL rabbits were divided into two groups. Group A (n =...
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Published in: | Proceedings of the National Academy of Sciences - PNAS 1987-08, Vol.84 (16), p.5928-5931 |
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creator | Kita, T Nagano, Y Yokode, M Ishii, K Kume, N Ooshima, A Yoshida, H Kawai, C |
description | In this study, we questioned whether in vivo probucol could prevent the progression of atherosclerosis in homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits, an animal model for familial hypercholesterolemia. At 2 months of age, eight WHHL rabbits were divided into two groups. Group A (n = 4) was fed standard rabbit chow for 6 months. Group B (n = 4) was fed standard rabbit chow containing 1% probucol for 6 months. At the end of the experiments, average plasma concentrations of cholesterol were 704 ± 121 mg/dl in group A and 584 ± 61 mg/dl in group B, respectively. The percentage of surface area of total thoracic aorta with visible plaques in group A versus group B was 54.2% ± 18.8% versus 7.0% ± 6.3%, respectively. What was noteworthy was that the percentage of plaque in the descending thoracic aorta was almost negligible (0.2% ± 0.2%) in group B rabbits compared to that in group A rabbits (41.1% ± 20.2%). Low density lipoproteins (LDL) isolated from WHHL rabbits under treatment with probucol (group B) were shown to be highly resistant to oxidative modification by cupric ion and to be minimally recognized by macrophages. On the contrary, LDL from group A rabbits incubated with cupric ion showed a 7.4-fold increase in peroxides (thiobarbituric acid-reactive substances) and a 4.3-fold increase in the synthesis of cholesteryl ester in macrophages compared to those of LDL from group B rabbits. Thus, probucol could definitely prevent the progression of atherosclerosis in homozygous WHHL rabbits in vivo by limiting oxidative LDL modification and foam cell transformation of macrophages. |
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At 2 months of age, eight WHHL rabbits were divided into two groups. Group A (n = 4) was fed standard rabbit chow for 6 months. Group B (n = 4) was fed standard rabbit chow containing 1% probucol for 6 months. At the end of the experiments, average plasma concentrations of cholesterol were 704 ± 121 mg/dl in group A and 584 ± 61 mg/dl in group B, respectively. The percentage of surface area of total thoracic aorta with visible plaques in group A versus group B was 54.2% ± 18.8% versus 7.0% ± 6.3%, respectively. What was noteworthy was that the percentage of plaque in the descending thoracic aorta was almost negligible (0.2% ± 0.2%) in group B rabbits compared to that in group A rabbits (41.1% ± 20.2%). Low density lipoproteins (LDL) isolated from WHHL rabbits under treatment with probucol (group B) were shown to be highly resistant to oxidative modification by cupric ion and to be minimally recognized by macrophages. On the contrary, LDL from group A rabbits incubated with cupric ion showed a 7.4-fold increase in peroxides (thiobarbituric acid-reactive substances) and a 4.3-fold increase in the synthesis of cholesteryl ester in macrophages compared to those of LDL from group B rabbits. Thus, probucol could definitely prevent the progression of atherosclerosis in homozygous WHHL rabbits in vivo by limiting oxidative LDL modification and foam cell transformation of macrophages.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.84.16.5928</identifier><identifier>PMID: 3475709</identifier><identifier>CODEN: PNASA6</identifier><language>eng</language><publisher>Washington, DC: National Academy of Sciences of the United States of America</publisher><subject>Animals ; Aorta ; Aorta, Thoracic - pathology ; ARTERIOSCLEROSE ; ARTERIOSCLEROSIS ; Arteriosclerosis - drug therapy ; Arteriosclerosis - etiology ; Arteriosclerosis - pathology ; Atherosclerosis ; Atherosclerotic plaque ; Biological and medical sciences ; CHOLESTEROL ; Cholesterol - blood ; Cholesterols ; COLESTEROL ; COMPOSE PHENOLIQUE ; COMPUESTOS FENOLICOS ; CONEJO (ORYCTOLAGUS) ; Disease Models, Animal ; Female ; Foam cells ; General and cellular metabolism. Vitamins ; Hyperlipoproteinemia Type II - complications ; Hyperlipoproteinemia Type II - pathology ; LAPIN ; Lipid Peroxides - metabolism ; LIPOPROTEINAS ; LIPOPROTEINE ; LIPOPROTEINS ; Lipoproteins - metabolism ; Macrophages ; Macrophages - metabolism ; Male ; Medical sciences ; METABOLIC DISORDERS ; Mice ; Pharmacology. Drug treatments ; PHENOLIC COMPOUNDS ; Phenols - therapeutic use ; Probucol - therapeutic use ; RABBITS ; Thoracic aorta ; TRASTORNOS METABOLICOS ; TROUBLE DU METABOLISME ; Xanthomatosis</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 1987-08, Vol.84 (16), p.5928-5931</ispartof><rights>1988 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c577t-9b6c0d6ef08bc2bfa6e85731ee6db9baf1159936c4b7acf0d057dda208e85e753</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/84/16.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/30153$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/30153$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,315,733,786,790,891,27957,27958,53827,53829,58593,58826</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7629107$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3475709$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kita, T</creatorcontrib><creatorcontrib>Nagano, Y</creatorcontrib><creatorcontrib>Yokode, M</creatorcontrib><creatorcontrib>Ishii, K</creatorcontrib><creatorcontrib>Kume, N</creatorcontrib><creatorcontrib>Ooshima, A</creatorcontrib><creatorcontrib>Yoshida, H</creatorcontrib><creatorcontrib>Kawai, C</creatorcontrib><title>Probucol prevents the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbit, an animal model for familial hypercholesterolemia</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>In this study, we questioned whether in vivo probucol could prevent the progression of atherosclerosis in homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits, an animal model for familial hypercholesterolemia. At 2 months of age, eight WHHL rabbits were divided into two groups. Group A (n = 4) was fed standard rabbit chow for 6 months. Group B (n = 4) was fed standard rabbit chow containing 1% probucol for 6 months. At the end of the experiments, average plasma concentrations of cholesterol were 704 ± 121 mg/dl in group A and 584 ± 61 mg/dl in group B, respectively. The percentage of surface area of total thoracic aorta with visible plaques in group A versus group B was 54.2% ± 18.8% versus 7.0% ± 6.3%, respectively. What was noteworthy was that the percentage of plaque in the descending thoracic aorta was almost negligible (0.2% ± 0.2%) in group B rabbits compared to that in group A rabbits (41.1% ± 20.2%). Low density lipoproteins (LDL) isolated from WHHL rabbits under treatment with probucol (group B) were shown to be highly resistant to oxidative modification by cupric ion and to be minimally recognized by macrophages. On the contrary, LDL from group A rabbits incubated with cupric ion showed a 7.4-fold increase in peroxides (thiobarbituric acid-reactive substances) and a 4.3-fold increase in the synthesis of cholesteryl ester in macrophages compared to those of LDL from group B rabbits. Thus, probucol could definitely prevent the progression of atherosclerosis in homozygous WHHL rabbits in vivo by limiting oxidative LDL modification and foam cell transformation of macrophages.</description><subject>Animals</subject><subject>Aorta</subject><subject>Aorta, Thoracic - pathology</subject><subject>ARTERIOSCLEROSE</subject><subject>ARTERIOSCLEROSIS</subject><subject>Arteriosclerosis - drug therapy</subject><subject>Arteriosclerosis - etiology</subject><subject>Arteriosclerosis - pathology</subject><subject>Atherosclerosis</subject><subject>Atherosclerotic plaque</subject><subject>Biological and medical sciences</subject><subject>CHOLESTEROL</subject><subject>Cholesterol - blood</subject><subject>Cholesterols</subject><subject>COLESTEROL</subject><subject>COMPOSE PHENOLIQUE</subject><subject>COMPUESTOS FENOLICOS</subject><subject>CONEJO (ORYCTOLAGUS)</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Foam cells</subject><subject>General and cellular metabolism. Vitamins</subject><subject>Hyperlipoproteinemia Type II - complications</subject><subject>Hyperlipoproteinemia Type II - pathology</subject><subject>LAPIN</subject><subject>Lipid Peroxides - metabolism</subject><subject>LIPOPROTEINAS</subject><subject>LIPOPROTEINE</subject><subject>LIPOPROTEINS</subject><subject>Lipoproteins - metabolism</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>METABOLIC DISORDERS</subject><subject>Mice</subject><subject>Pharmacology. Drug treatments</subject><subject>PHENOLIC COMPOUNDS</subject><subject>Phenols - therapeutic use</subject><subject>Probucol - therapeutic use</subject><subject>RABBITS</subject><subject>Thoracic aorta</subject><subject>TRASTORNOS METABOLICOS</subject><subject>TROUBLE DU METABOLISME</subject><subject>Xanthomatosis</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><recordid>eNp9kUuLFDEUhYMoY9u6FkQlC9GN3ZN6Jlm4kMEXDCjo4DLcpJLuDKlKTVI9OL_DP-wtu22djVBUpXK-c-9JLiGPC7YuGK9OxwHyWtTrol03shR3yKJgsli1tWR3yYKxkq9EXdb3yYOcLxljshHshJxUNW84kwvy80uKemdioGOy13aYMp22Fn_iJtmcfRxodBRwL8Vswvz2mfqBfocJBtCWouIn0AFXN6NNwY--s703NIHWfnpNYcDH9xBoHzsbqIuJOuh98Lj122O2Mdg8YfGATnhI7jkI2T46fJfk4v27b2cfV-efP3w6e3u-Mg3n00rq1rCutY4JbUrtoLWi4VVhbdtpqcEVRSNl1ZpaczCOdazhXQclE8hZ3lRL8mZfd9zp3nYGT58gqDFh2HSjInh1Wxn8Vm3itSqlkLxF_8uDP8WrHR5A9T4bGwIMNu6y4rwta7xvBE_3oMHry8m6Y4-CqXmMah6jErUqWjWPER3P_o125A9zQ_3FQYdsILgEg_H5iGFjOdddkucHbK7_R73V59V_AeV2IUz2x4Tkkz15maeY_gZiRVOh-HQvOogKNgmjXHwVGLWUUojqF46Y1j0</recordid><startdate>19870801</startdate><enddate>19870801</enddate><creator>Kita, T</creator><creator>Nagano, Y</creator><creator>Yokode, M</creator><creator>Ishii, K</creator><creator>Kume, N</creator><creator>Ooshima, A</creator><creator>Yoshida, H</creator><creator>Kawai, C</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</general><scope>FBQ</scope><scope>IQODW</scope><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>19870801</creationdate><title>Probucol prevents the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbit, an animal model for familial hypercholesterolemia</title><author>Kita, T ; Nagano, Y ; Yokode, M ; Ishii, K ; Kume, N ; Ooshima, A ; Yoshida, H ; Kawai, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c577t-9b6c0d6ef08bc2bfa6e85731ee6db9baf1159936c4b7acf0d057dda208e85e753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>Animals</topic><topic>Aorta</topic><topic>Aorta, Thoracic - pathology</topic><topic>ARTERIOSCLEROSE</topic><topic>ARTERIOSCLEROSIS</topic><topic>Arteriosclerosis - drug therapy</topic><topic>Arteriosclerosis - etiology</topic><topic>Arteriosclerosis - pathology</topic><topic>Atherosclerosis</topic><topic>Atherosclerotic plaque</topic><topic>Biological and medical sciences</topic><topic>CHOLESTEROL</topic><topic>Cholesterol - blood</topic><topic>Cholesterols</topic><topic>COLESTEROL</topic><topic>COMPOSE PHENOLIQUE</topic><topic>COMPUESTOS FENOLICOS</topic><topic>CONEJO (ORYCTOLAGUS)</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Foam cells</topic><topic>General and cellular metabolism. Vitamins</topic><topic>Hyperlipoproteinemia Type II - complications</topic><topic>Hyperlipoproteinemia Type II - pathology</topic><topic>LAPIN</topic><topic>Lipid Peroxides - metabolism</topic><topic>LIPOPROTEINAS</topic><topic>LIPOPROTEINE</topic><topic>LIPOPROTEINS</topic><topic>Lipoproteins - metabolism</topic><topic>Macrophages</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>METABOLIC DISORDERS</topic><topic>Mice</topic><topic>Pharmacology. Drug treatments</topic><topic>PHENOLIC COMPOUNDS</topic><topic>Phenols - therapeutic use</topic><topic>Probucol - therapeutic use</topic><topic>RABBITS</topic><topic>Thoracic aorta</topic><topic>TRASTORNOS METABOLICOS</topic><topic>TROUBLE DU METABOLISME</topic><topic>Xanthomatosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kita, T</creatorcontrib><creatorcontrib>Nagano, Y</creatorcontrib><creatorcontrib>Yokode, M</creatorcontrib><creatorcontrib>Ishii, K</creatorcontrib><creatorcontrib>Kume, N</creatorcontrib><creatorcontrib>Ooshima, A</creatorcontrib><creatorcontrib>Yoshida, H</creatorcontrib><creatorcontrib>Kawai, C</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kita, T</au><au>Nagano, Y</au><au>Yokode, M</au><au>Ishii, K</au><au>Kume, N</au><au>Ooshima, A</au><au>Yoshida, H</au><au>Kawai, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Probucol prevents the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbit, an animal model for familial hypercholesterolemia</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>1987-08-01</date><risdate>1987</risdate><volume>84</volume><issue>16</issue><spage>5928</spage><epage>5931</epage><pages>5928-5931</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><coden>PNASA6</coden><notes>875729988</notes><notes>L74</notes><notes>S30</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>In this study, we questioned whether in vivo probucol could prevent the progression of atherosclerosis in homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits, an animal model for familial hypercholesterolemia. At 2 months of age, eight WHHL rabbits were divided into two groups. Group A (n = 4) was fed standard rabbit chow for 6 months. Group B (n = 4) was fed standard rabbit chow containing 1% probucol for 6 months. At the end of the experiments, average plasma concentrations of cholesterol were 704 ± 121 mg/dl in group A and 584 ± 61 mg/dl in group B, respectively. The percentage of surface area of total thoracic aorta with visible plaques in group A versus group B was 54.2% ± 18.8% versus 7.0% ± 6.3%, respectively. What was noteworthy was that the percentage of plaque in the descending thoracic aorta was almost negligible (0.2% ± 0.2%) in group B rabbits compared to that in group A rabbits (41.1% ± 20.2%). Low density lipoproteins (LDL) isolated from WHHL rabbits under treatment with probucol (group B) were shown to be highly resistant to oxidative modification by cupric ion and to be minimally recognized by macrophages. On the contrary, LDL from group A rabbits incubated with cupric ion showed a 7.4-fold increase in peroxides (thiobarbituric acid-reactive substances) and a 4.3-fold increase in the synthesis of cholesteryl ester in macrophages compared to those of LDL from group B rabbits. Thus, probucol could definitely prevent the progression of atherosclerosis in homozygous WHHL rabbits in vivo by limiting oxidative LDL modification and foam cell transformation of macrophages.</abstract><cop>Washington, DC</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>3475709</pmid><doi>10.1073/pnas.84.16.5928</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Aorta Aorta, Thoracic - pathology ARTERIOSCLEROSE ARTERIOSCLEROSIS Arteriosclerosis - drug therapy Arteriosclerosis - etiology Arteriosclerosis - pathology Atherosclerosis Atherosclerotic plaque Biological and medical sciences CHOLESTEROL Cholesterol - blood Cholesterols COLESTEROL COMPOSE PHENOLIQUE COMPUESTOS FENOLICOS CONEJO (ORYCTOLAGUS) Disease Models, Animal Female Foam cells General and cellular metabolism. Vitamins Hyperlipoproteinemia Type II - complications Hyperlipoproteinemia Type II - pathology LAPIN Lipid Peroxides - metabolism LIPOPROTEINAS LIPOPROTEINE LIPOPROTEINS Lipoproteins - metabolism Macrophages Macrophages - metabolism Male Medical sciences METABOLIC DISORDERS Mice Pharmacology. Drug treatments PHENOLIC COMPOUNDS Phenols - therapeutic use Probucol - therapeutic use RABBITS Thoracic aorta TRASTORNOS METABOLICOS TROUBLE DU METABOLISME Xanthomatosis |
title | Probucol prevents the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbit, an animal model for familial hypercholesterolemia |
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