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- Publisher Website: 10.1016/S0021-9150(97)00185-8
- Scopus: eid_2-s2.0-0031822451
- PMID: 9544730
- WOS: WOS:000072378900006
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Article: Oxidized cholesterol in oxidized low density lipoprotein may be responsible for the inhibition of LPS-induced nitric oxide production in macrophages
Title | Oxidized cholesterol in oxidized low density lipoprotein may be responsible for the inhibition of LPS-induced nitric oxide production in macrophages |
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Authors | |
Keywords | J774.A1 Lipopolysaccharide Nitric oxide Oxidized cholesterol Oxidized LDL |
Issue Date | 1998 |
Publisher | Elsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis |
Citation | Atherosclerosis, 1998, v. 136 n. 1, p. 43-49 How to Cite? |
Abstract | Previous work has shown that oxidized low density lipoprotein (Ox-LDL) inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) production in macrophages. In this paper, the role of different components of Ox-LDL in the inhibitory effect was studied by measuring nitrite in media. Ox-LDL inhibited LPS-induced NO production in macrophage cell line J774.A1. When compared with Ox-LDL, native and acetylated LDL had a lesser effect on NO production. Pre- clearance of lipid hydroperoxides (LOOH) in Ox-LDL and removal of soluble thiobarbituric acid reactive substances (TBARS) in Ox-LDL solution by dialysis had no influence on the inhibitory effect Of Ox-LDL. The protein moiety of Ox-LDL had no effect on NO production, but the lipid moiety inhibited NO production to about the same extent as intact Ox-LDL. Linoleic acid and phosphatidylcholine, the main components of LDL lipid, whether oxidized separately or together, had no effect On NO production. However, if linoleic acid and cholesterol oxidized together, there was very strong inhibition of NO production. Cholesterol oxidized alone also had some inhibitory effect. These results suggest that oxidized cholesterol in Ox-LDL might be responsible for the inhibition of NO production in macrophages. |
Persistent Identifier | http://hdl.handle.net/10722/178621 |
ISSN | 2023 Impact Factor: 4.9 2023 SCImago Journal Rankings: 1.461 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Liu, SX | en_US |
dc.contributor.author | Chen, Y | en_US |
dc.contributor.author | Zhou, M | en_US |
dc.contributor.author | Wan, J | en_US |
dc.date.accessioned | 2012-12-19T09:48:46Z | - |
dc.date.available | 2012-12-19T09:48:46Z | - |
dc.date.issued | 1998 | en_US |
dc.identifier.citation | Atherosclerosis, 1998, v. 136 n. 1, p. 43-49 | en_US |
dc.identifier.issn | 0021-9150 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/178621 | - |
dc.description.abstract | Previous work has shown that oxidized low density lipoprotein (Ox-LDL) inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) production in macrophages. In this paper, the role of different components of Ox-LDL in the inhibitory effect was studied by measuring nitrite in media. Ox-LDL inhibited LPS-induced NO production in macrophage cell line J774.A1. When compared with Ox-LDL, native and acetylated LDL had a lesser effect on NO production. Pre- clearance of lipid hydroperoxides (LOOH) in Ox-LDL and removal of soluble thiobarbituric acid reactive substances (TBARS) in Ox-LDL solution by dialysis had no influence on the inhibitory effect Of Ox-LDL. The protein moiety of Ox-LDL had no effect on NO production, but the lipid moiety inhibited NO production to about the same extent as intact Ox-LDL. Linoleic acid and phosphatidylcholine, the main components of LDL lipid, whether oxidized separately or together, had no effect On NO production. However, if linoleic acid and cholesterol oxidized together, there was very strong inhibition of NO production. Cholesterol oxidized alone also had some inhibitory effect. These results suggest that oxidized cholesterol in Ox-LDL might be responsible for the inhibition of NO production in macrophages. | en_US |
dc.language | eng | en_US |
dc.publisher | Elsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis | en_US |
dc.relation.ispartof | Atherosclerosis | en_US |
dc.subject | J774.A1 | - |
dc.subject | Lipopolysaccharide | - |
dc.subject | Nitric oxide | - |
dc.subject | Oxidized cholesterol | - |
dc.subject | Oxidized LDL | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Cell Line | en_US |
dc.subject.mesh | Cholesterol - Metabolism | en_US |
dc.subject.mesh | Linoleic Acid - Metabolism | en_US |
dc.subject.mesh | Lipopolysaccharides - Pharmacology | en_US |
dc.subject.mesh | Lipoproteins, Ldl - Metabolism | en_US |
dc.subject.mesh | Macrophages - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Nitric Oxide - Biosynthesis | en_US |
dc.subject.mesh | Oxidation-Reduction | en_US |
dc.subject.mesh | Phosphatidylcholines - Metabolism | en_US |
dc.subject.mesh | Thiobarbituric Acid Reactive Substances - Metabolism | en_US |
dc.title | Oxidized cholesterol in oxidized low density lipoprotein may be responsible for the inhibition of LPS-induced nitric oxide production in macrophages | 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.doi | 10.1016/S0021-9150(97)00185-8 | en_US |
dc.identifier.pmid | 9544730 | - |
dc.identifier.scopus | eid_2-s2.0-0031822451 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0031822451&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 136 | en_US |
dc.identifier.issue | 1 | en_US |
dc.identifier.spage | 43 | en_US |
dc.identifier.epage | 49 | en_US |
dc.identifier.isi | WOS:000072378900006 | - |
dc.publisher.place | Ireland | en_US |
dc.identifier.scopusauthorid | Liu, SX=7409463469 | en_US |
dc.identifier.scopusauthorid | Chen, Y=16745998900 | en_US |
dc.identifier.scopusauthorid | Zhou, M=7403506134 | en_US |
dc.identifier.scopusauthorid | Wan, J=8930305000 | en_US |
dc.identifier.issnl | 0021-9150 | - |