Document Detail

PSK protects macrophages from lipoperoxide accumulation and foam cell formation caused by oxidatively modified low-density lipoprotein.
MedLine Citation:
PMID:  8830930     Owner:  NLM     Status:  MEDLINE    
In previous works, it has been evidenced that lipoperoxidative injury to macrophages caused by oxidatively modified low-density lipoprotein (O-LDL) plays an important role in foam cell formation, and that PSK, a protein bound polysaccharide extracted from the class Basidiomycetes Coriolus Versicolor, can protect macrophages from lipoperoxidative injury induced by tert-butyl hydroperoxide (tbOOH). In this paper PSK protection of macrophages from lipoperoxide (LPO) accumulation and foam cell formation caused by O-LDL and its action mechanism were further studied. The LPO accumulation was determined by using ACAS 570. Dynamic assay of the LPO level in eight single cells after adding O-LDL or determination of the average LPO content in a lot of cells incubated in advance with O-LDL for 12 h, both indicated that O-LDL might induce LPO accumulation in macrophages and the effects of O-LDL could be prevented by PSK. O-LDL might cause the changes of morphological structure in macrophages and the transformation of macrophages into foam cells, and the effects could also be prevented by PSK. The determination of selenium-dependent glutathione peroxidase (SeGSHPx) activities and mRNA contents of macrophages and changes of SeGSHPx activity and mRNA content after incubation with tbOOH showed that PSK might increase the SeGSHPx activity of macrophage and the enhanced SeGSHPx activity may occur at the level of gene transcription.
C Yuan; Z Mei; S Liu; L Yi
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Atherosclerosis     Volume:  124     ISSN:  0021-9150     ISO Abbreviation:  Atherosclerosis     Publication Date:  1996 Aug 
Date Detail:
Created Date:  1996-12-11     Completed Date:  1996-12-11     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0242543     Medline TA:  Atherosclerosis     Country:  IRELAND    
Other Details:
Languages:  eng     Pagination:  171-81     Citation Subset:  IM    
Research Laboratory of Free Radical Medicine, First Military Medical University, Guangzhou, China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Arteriosclerosis / metabolism,  pathology,  prevention & control
Foam Cells / drug effects*,  metabolism,  pathology
Glutathione Peroxidase / drug effects,  genetics,  metabolism
Immunologic Factors / pharmacology*
Lipid Peroxides / metabolism*
Lipoproteins, LDL / drug effects*,  metabolism
Macrophages / metabolism*
Peroxides / adverse effects
Proteoglycans / pharmacology*
RNA, Messenger / analysis
Reg. No./Substance:
0/Immunologic Factors; 0/Lipid Peroxides; 0/Lipoproteins, LDL; 0/Peroxides; 0/Proteoglycans; 0/RNA, Messenger; 66455-27-4/krestin; 75-91-2/tert-Butylhydroperoxide; EC Peroxidase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Enhanced capacity of n-3 fatty acid-enriched macrophages to oxidize low density lipoprotein mechanis...
Next Document:  Apolipoprotein E1-Hammersmith (Lys146-->Asn;Arg147-->Trp), due to a dinucleotide substitution, is as...