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Article: The polysaccharide krestin prevents plaque formation in experimentally atherosclerotic rabbits

TitleThe polysaccharide krestin prevents plaque formation in experimentally atherosclerotic rabbits
Authors
KeywordsAntioxidation
Atherosclerosis
Krestin
Plaque
Polysaccharide
Issue Date1997
PublisherChapman & Hall, Journals Department. The Journal's web site is located at http://www.chaphall.com/chaphall/journals.html
Citation
Medical Science Research, 1997, v. 25 n. 5, p. 297-300 How to Cite?
AbstractOur previous studies showed that lipoperoxidative injury is a major cause of the transformation of macrophages into foam cells induced by oxidatively modified low density lipoprotein (O-LDL), and that the polysaccharide krestin (PSK), administered intraperitoneally to mice, enhanced selenium-dependent glutathione peroxidase gene expression in macrophages, protected in vitro macrophages from foam cell formation caused by O-LDL and prevented lipoperoxidative injury to experimentally atherosclerotic rabbits. The aim of the present study was to determine whether PSK could prevent plaque formation in experimentally atherosclerotic rabbits. The plaque area of the aorta in a given PSK group was 69.9% lower than in the control group. The percentage of plaque formation at the opening of arteries in the abdominal aorta was relatively much lower in the PSK group (28.9% vs 71.0%). Stenosis of the coronary artery branches in the heart wall of the PSK group was also milder than in the control group. Prevention of the transformation of macrophages into foam cells by elevation of their antioxidation potential may be another important means to prevent atherosclerosis, different from that of antioxidants given to inhibit LDL oxidation.
Persistent Identifierhttp://hdl.handle.net/10722/178609
ISSN
2001 Impact Factor: 0.384
2003 SCImago Journal Rankings: 0.107
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Yen_US
dc.contributor.authorZhou, Men_US
dc.contributor.authorLou, Nen_US
dc.contributor.authorLiu, Sen_US
dc.contributor.authorPang, Zen_US
dc.contributor.authorWan, Jen_US
dc.date.accessioned2012-12-19T09:48:40Z-
dc.date.available2012-12-19T09:48:40Z-
dc.date.issued1997en_US
dc.identifier.citationMedical Science Research, 1997, v. 25 n. 5, p. 297-300en_US
dc.identifier.issn0269-8951en_US
dc.identifier.urihttp://hdl.handle.net/10722/178609-
dc.description.abstractOur previous studies showed that lipoperoxidative injury is a major cause of the transformation of macrophages into foam cells induced by oxidatively modified low density lipoprotein (O-LDL), and that the polysaccharide krestin (PSK), administered intraperitoneally to mice, enhanced selenium-dependent glutathione peroxidase gene expression in macrophages, protected in vitro macrophages from foam cell formation caused by O-LDL and prevented lipoperoxidative injury to experimentally atherosclerotic rabbits. The aim of the present study was to determine whether PSK could prevent plaque formation in experimentally atherosclerotic rabbits. The plaque area of the aorta in a given PSK group was 69.9% lower than in the control group. The percentage of plaque formation at the opening of arteries in the abdominal aorta was relatively much lower in the PSK group (28.9% vs 71.0%). Stenosis of the coronary artery branches in the heart wall of the PSK group was also milder than in the control group. Prevention of the transformation of macrophages into foam cells by elevation of their antioxidation potential may be another important means to prevent atherosclerosis, different from that of antioxidants given to inhibit LDL oxidation.en_US
dc.languageengen_US
dc.publisherChapman & Hall, Journals Department. The Journal's web site is located at http://www.chaphall.com/chaphall/journals.htmlen_US
dc.relation.ispartofMedical Science Researchen_US
dc.subjectAntioxidationen_US
dc.subjectAtherosclerosisen_US
dc.subjectKrestinen_US
dc.subjectPlaqueen_US
dc.subjectPolysaccharideen_US
dc.titleThe polysaccharide krestin prevents plaque formation in experimentally atherosclerotic rabbitsen_US
dc.typeArticleen_US
dc.identifier.emailWan, J: jmfwan@hku.hken_US
dc.identifier.authorityWan, J=rp00798en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-0031000391en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031000391&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume25en_US
dc.identifier.issue5en_US
dc.identifier.spage297en_US
dc.identifier.epage300en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridChen, Y=16745998900en_US
dc.identifier.scopusauthoridZhou, M=7403506134en_US
dc.identifier.scopusauthoridLou, N=7006629613en_US
dc.identifier.scopusauthoridLiu, S=7409463469en_US
dc.identifier.scopusauthoridPang, Z=7103343225en_US
dc.identifier.scopusauthoridWan, J=8930305000en_US

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