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PSK protects macrophages from lipoperoxide accumulation and foam cell formation caused by oxidatively modified
1Research Laboratory of Free Radical Medicine, First Military Medical University, Guangzhou, China.
Abstract:
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.
Insights
PSK protects macrophages from foam cell formation by preventing lipoperoxide accumulation. This protein-bound polysaccharide enhances selenium-dependent glutathione peroxidase activity, potentially at the gene transcription level.
Area of Science:
- Biochemistry
- Cell Biology
- Immunology
Background:
- Oxidatively modified low-density lipoprotein (O-LDL) induces lipoperoxidative injury in macrophages, contributing to foam cell formation.
- PSK, a polysaccharide from Coriolus Versicolor, previously showed protective effects against tert-butyl hydroperoxide (tbOOH)-induced injury.
Purpose of the Study:
- To investigate PSK's protective mechanisms against O-LDL-induced lipoperoxide (LPO) accumulation and foam cell formation in macrophages.
- To elucidate the role of PSK in modulating cellular antioxidant defense systems.
Main Methods:
- Lipoperoxide (LPO) accumulation was quantified using ACAS 570.
- Macrophage morphology and foam cell transformation were assessed.
- Selenium-dependent glutathione peroxidase (SeGSHPx) activity and mRNA levels were determined.
Main Results:
- O-LDL induced LPO accumulation and foam cell formation in macrophages, effects prevented by PSK.
- PSK treatment prevented O-LDL-induced morphological changes and foam cell transformation.
- PSK increased SeGSHPx activity and mRNA content in macrophages, suggesting transcriptional regulation.
Conclusions:
- PSK effectively protects macrophages from O-LDL-induced lipotoxicity and foam cell formation.
- PSK enhances macrophage antioxidant capacity by upregulating SeGSHPx, likely via gene transcription.
- PSK represents a potential therapeutic agent for conditions involving O-LDL-induced macrophage damage.