L-cystathionine inhibits oxidized low density lipoprotein-induced THP-1-derived macrophage inflammatory cytokine monocyte chemoattractant protein-1 generation via the NF-kappa B pathwayVisa övriga samt affilieringar
2015 (Engelska)Ingår i: Scientific Reports, E-ISSN 2045-2322, Vol. 5, nr 10453Artikel i tidskrift (Refereegranskat) Published
Abstract [en]
This study aimed to explore whether and how L-cystathionine had any regulatory effect on the inflammatory response in THP-1-derived macrophages cultured in vitro under oxidized low-density lipoprotein (ox-LDL) stimulation. The human monocyte line THP-1 cell was cultured in vitro and differentiated into macrophages after 24 hours of PMA induction. Macrophages were pretreated with L-cystathionine and then treated with ox-LDL. The results showed that compared with the controls, ox-LDL stimulation significantly upregulated the expression of THP-1-derived macrophage MCP-1 by enhancing NF-kappa B p65 phosphorylation, nuclear translocation and DNA binding with the MCP-1 promoter. Compared with the ox-LDL group, 0.3 mmol/L and 1.0 mmol/L L-cystathionine significantly inhibited the expression of THP-1-derived macrophage MCP-1. Mechanistically, 0.3 mmol/L and 1.0 mmol/L L-cystathionine suppressed phosphorylation and nuclear translocation of the NF-kappa B p65 protein, as well as the DNA binding activity and DNA binding level of NF-kappa B with the MCP-1 promoter, which resulted in a reduced THP-1-derived macrophage MCP-1 generation. This study suggests that L-cystathionine could inhibit the expression of MCP-1 in THP-1-derived macrophages induced by ox-LDL via inhibition of NF-kappa B p65 phosphorylation, nuclear translocation, and binding of the MCP-1 promoter sequence after entry into the nucleus.
Ort, förlag, år, upplaga, sidor
Nature Publishing Group: Open Access Journals - Option C / Nature Publishing Group , 2015. Vol. 5, nr 10453
Nationell ämneskategori
Medicinska och farmaceutiska grundvetenskaper
Identifikatorer
URN: urn:nbn:se:liu:diva-119584DOI: 10.1038/srep10453ISI: 000355546600001PubMedID: 26020416OAI: oai:DiVA.org:liu-119584DiVA, id: diva2:825171
Anmärkning
Funding Agencies|National Natural Science Foundation of China [31130030, 81370154, 91439110]; Major Basic Research Project of China [2012CB517806, 2011CB503904]; Program for New Century Excellent Talents of Ministry of Education, China [NCET-11-0005]
2015-06-232015-06-222022-09-15