title: Salicylideneamino-2-thiophenol inhibits inflammatory mediator genes (RANTES, MCP-1, IL-8 and HIF-1alpha) expression induced by tert-butyl hydroperoxide via MAPK pathways in rat peritoneal macrophages.
abstract: Salicylideneamino-2-thiophenol (Sal) regulated the redox status and the expression of chemokines induced by tert-butyl hydroperoxide (t-BHP). Sal (100 microM) increased reduced/oxidized glutathione (GSH/GSSG) ratios and thiol (SH) levels by 210 and 157%, respectively, and decreased reactive oxygen species (ROS) levels by 60% in t-BHP-treated macrophages. The inductions of regulated upon activation, normal T-cell expressed and secreted (RANTES), monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8) and hypoxia inducible factor-1alpha (HIF-1alpha) by t-BHP (10 microM) were decreased to 250, 80, 80 and 500% by Sal (100 microM), respectively. In the Sal signaling pathway, c-Jun N-terminal kinases (JNK), extracellular signal-regulated kinases (ERK) and p38 signaling protein modulation were decreased by 67, 69 and 119%, respectively, by Sal at 100 microM. Sal (100 microM) also altered cytosol and nuclear NF-kappaB protein expression by 169 and 5%, respectively. Sal also attenuated NF-kappaB nuclear binding activity. Sal thus has a protective effect against t-BHP-induced inflammation and that this, in part, is due to the inhibition of the production of RANTES, MCP-1, IL-8 and HIF-1alpha via the modulation of the NF-kappaB and mitogen-activated protein kinase (MAPK) pathways.
authors.affiliation: Department of Microbiology, School of Dentistry and Research Institute for Oral Biotechnology, Busan, Korea.
authors.forename: Jin
authors.initials: J
authors.lastname: Chung
authors.forename: Hwa Sun
authors.initials: HS
authors.lastname: Lee
authors.forename: Hae Young
authors.initials: HY
authors.lastname: Chung
authors.forename: Taek Rim
authors.initials: TR
authors.lastname: Yoon
authors.forename: Hyung Keun
authors.initials: HK
authors.lastname: Kim
mesh_terms: D000818:Animals; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D018946:Chemokine CCL5 / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D005978:Glutathione / Q000378:metabolism; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics / Q000378:metabolism; D007249:Inflammation / Q000235:genetics*; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D017737:Macrophages, Peritoneal / Q000187:drug effects* / Q000201:enzymology*; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism; D010636:Phenols / Q000737:chemistry / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D012459:Salicylates / Q000737:chemistry / Q000494:pharmacology*; D020156:Salicylic Acid / Q000737:chemistry; D013438:Sulfhydryl Compounds / Q000737:chemistry / Q000494:pharmacology*; D020122:tert-Butylhydroperoxide / Q000494:pharmacology*
chemical_list: D018932:Chemokine CCL2; D018946:Chemokine CCL5; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D016209:Interleukin-8; D016328:NF-kappa B; D010636:Phenols; D012333:RNA, Messenger; D012459:Salicylates; D013438:Sulfhydryl Compounds; C532534:salicylideneamino-2-thiophenol; C042983:thiophenol; D020122:tert-Butylhydroperoxide; D020928:Mitogen-Activated Protein Kinases; D005978:Glutathione; D020156:Salicylic Acid