Y. Chen et al., PSK PROTECTS MACROPHAGES FROM LIPOPEROXIDE ACCUMULATION AND FOAM CELL-FORMATION CAUSED BY OXIDATIVELY MODIFIED LOW-DENSITY-LIPOPROTEIN, Atherosclerosis, 124(2), 1996, pp. 171-181
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 in
jury induced by tert-butyl hydroperoxide (tbOOH). In this paper PSK pr
otection of macrophages from lipoperoxide (LPO) accumulation and foam
cell formation caused by O-LDL and its action mechanism were further s
tudied, The LPO accumulation was determined by using ACAS 570. Dynamic
assay of the LPO level in eight single cells after adding O-LDL or de
termination 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 LP
O accumulation in macrophages and the effects of O-LDL could be preven
ted by PSK. O-LDL might cause the changes of morphological structure i
n macrophages and the transformation of macrophages into foam cells, a
nd the effects could also be prevented by PSK, The determination of, s
elenium-dependent glutathione peroxidase (SeGSHPx) activities and mRNA
contents of macrophages and changes of SeGSHPx activity and mRNA cont
ent after incubation with tbOOH showed that PSK might increase the SeG
SHPx activity of macrophage and the enhanced SeGSHPx activity may occu
r at the level of gene transcription.