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Article: Damage to macrophages by tert-butyl hydroperoxide and the protective action of the protein bound polysaccharide krestin
Title | Damage to macrophages by tert-butyl hydroperoxide and the protective action of the protein bound polysaccharide krestin |
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Authors | |
Keywords | Glutathione Peroxidase Macrophage Manganese Superoxide Dismutase Non-Selenium Dependent Glutathione Peroxidase Polysaccharide Krestin Selenium Dependent Glutathione Peroxidase Tert-Butyl Hydroperoxide |
Issue Date | 1997 |
Publisher | Chapman & 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. 9, p. 601-606 How to Cite? |
Abstract | Previous work has shown that lipoperoxidative damage to macrophages caused by oxidatively modified low-density lipoprotein (O-LDL) plays an important role in foam cell formation, and that the polysaccharide krestin (PSK), a protein-bound polysaccharide extracted from Coriolus versicolor, can protect macrophages from foam cell formation caused by O-LDL and from damage to physiological functions induced by tert-butyl hydroperoxide (tbOOH). In order to demonstrate further the mechanism of lipoperoxidative damage in foam cell formation caused by O-LDL, we investigated the damage to macrophage ultrastructure induced by tbOOH, protection by PSK and its action mechanism. Macrophages incubated with tbOOH showed morphological changes under the transmission electron and scanning electron microscope, their survival rate was decreased markedly, and the effects could be prevented and alleviated by PSK. As compared with a non-PSK treated group, selenium dependent glutathione peroxidase (SeGSHPx) and non-selenium dependent glutathione peroxidase (non-SeGSHPx) activities, manganese superoxide dismutase (MnSOD) activity and mRNA content increased significantly in the PSK-treated group. These findings and previous studies taken together suggest that protection by PSK is due to the induction of gene expression of antioxidative enzymes, SeGSHPx, non-SeGSHPx and MnSOD, in the macrophages. |
Persistent Identifier | http://hdl.handle.net/10722/178602 |
ISSN | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chen, Y | en_US |
dc.contributor.author | Zhou, M | en_US |
dc.contributor.author | Guo, Z | en_US |
dc.contributor.author | Liu, S | en_US |
dc.contributor.author | Pang, Z | en_US |
dc.contributor.author | Sun, J | en_US |
dc.contributor.author | Lou, K | en_US |
dc.contributor.author | Wan, J | en_US |
dc.date.accessioned | 2012-12-19T09:48:37Z | - |
dc.date.available | 2012-12-19T09:48:37Z | - |
dc.date.issued | 1997 | en_US |
dc.identifier.citation | Medical Science Research, 1997, v. 25 n. 9, p. 601-606 | en_US |
dc.identifier.issn | 0269-8951 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/178602 | - |
dc.description.abstract | Previous work has shown that lipoperoxidative damage to macrophages caused by oxidatively modified low-density lipoprotein (O-LDL) plays an important role in foam cell formation, and that the polysaccharide krestin (PSK), a protein-bound polysaccharide extracted from Coriolus versicolor, can protect macrophages from foam cell formation caused by O-LDL and from damage to physiological functions induced by tert-butyl hydroperoxide (tbOOH). In order to demonstrate further the mechanism of lipoperoxidative damage in foam cell formation caused by O-LDL, we investigated the damage to macrophage ultrastructure induced by tbOOH, protection by PSK and its action mechanism. Macrophages incubated with tbOOH showed morphological changes under the transmission electron and scanning electron microscope, their survival rate was decreased markedly, and the effects could be prevented and alleviated by PSK. As compared with a non-PSK treated group, selenium dependent glutathione peroxidase (SeGSHPx) and non-selenium dependent glutathione peroxidase (non-SeGSHPx) activities, manganese superoxide dismutase (MnSOD) activity and mRNA content increased significantly in the PSK-treated group. These findings and previous studies taken together suggest that protection by PSK is due to the induction of gene expression of antioxidative enzymes, SeGSHPx, non-SeGSHPx and MnSOD, in the macrophages. | en_US |
dc.language | eng | en_US |
dc.publisher | Chapman & Hall, Journals Department. The Journal's web site is located at http://www.chaphall.com/chaphall/journals.html | en_US |
dc.relation.ispartof | Medical Science Research | en_US |
dc.subject | Glutathione Peroxidase | en_US |
dc.subject | Macrophage | en_US |
dc.subject | Manganese Superoxide Dismutase | en_US |
dc.subject | Non-Selenium Dependent Glutathione Peroxidase | en_US |
dc.subject | Polysaccharide Krestin | en_US |
dc.subject | Selenium Dependent Glutathione Peroxidase | en_US |
dc.subject | Tert-Butyl Hydroperoxide | en_US |
dc.title | Damage to macrophages by tert-butyl hydroperoxide and the protective action of the protein bound polysaccharide krestin | en_US |
dc.type | Article | en_US |
dc.identifier.email | Wan, J: jmfwan@hku.hk | en_US |
dc.identifier.authority | Wan, J=rp00798 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.scopus | eid_2-s2.0-0030830092 | en_US |
dc.identifier.hkuros | 35641 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0030830092&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 25 | en_US |
dc.identifier.issue | 9 | en_US |
dc.identifier.spage | 601 | en_US |
dc.identifier.epage | 606 | en_US |
dc.publisher.place | United Kingdom | en_US |
dc.identifier.scopusauthorid | Chen, Y=16745998900 | en_US |
dc.identifier.scopusauthorid | Zhou, M=7403506134 | en_US |
dc.identifier.scopusauthorid | Guo, Z=55227962300 | en_US |
dc.identifier.scopusauthorid | Liu, S=7409463469 | en_US |
dc.identifier.scopusauthorid | Pang, Z=7103343225 | en_US |
dc.identifier.scopusauthorid | Sun, J=35175139900 | en_US |
dc.identifier.scopusauthorid | Lou, K=7006629613 | en_US |
dc.identifier.scopusauthorid | Wan, J=8930305000 | en_US |
dc.identifier.issnl | 0269-8951 | - |