title: SeMet mediates anti-inflammation in LPS-induced U937 cells targeting NF-κB signaling pathway.
abstract: In previous studies, selenium (Se) was reported to play critical roles in anti-inflammatory activities. Nevertheless, limited information could be obtained during inflammation about selenomethionine (SeMet) in U937 human macrophage cells. The purpose of this study was to investigate the effects of SeMet on the inflammatory responses to lipopolysaccharide (LPS)-induced U937 macrophage cells and the signaling pathways targeted. U937 cells were pretreated with SeMet (1 μM) and subsequently induced with LPS (1 μg/ml) for 24 h. In the cell counting kit-8 assay (CCK-8), SeMet significantly inhibits the proliferation of U937 cells. SeMet also inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2) stimulated by LPS. In the Western blot assay and real-time polymerase chain reaction (RT-PCR), SeMet significantly reduced protein expression and production of inducible NO synthase (iNOS), tumor necrosis factor-alpha (TNF-α), and COX-2 in U937 cells. Furthermore, SeMet markedly suppressed the LPS-mediated activation of nuclear factor-kappa B (NF-κB) by blocking the degradation of inhibitor-κB proteins (IκBα) and lessening the translocations of P50 subunit content of NF-κB in the nucleus. These findings suggested the anti-inflammatory activity of SeMet in U937 cells; indicating that SeMet might be a potential treatment for inflammation therapy.
authors.affiliation: Department of Orthopedic Surgery, School of Medicine, The Second Affiliated Hospital, Zhejiang University, 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China, shenyue@zju.edu.cn.
authors.forename: Yue
authors.initials: Y
authors.lastname: Shen
authors.forename: Shizhou
authors.initials: S
authors.lastname: Yang
authors.forename: Zhongli
authors.initials: Z
authors.lastname: Shi
authors.forename: Tiao
authors.initials: T
authors.lastname: Lin
authors.forename: Hanxiao
authors.initials: H
authors.lastname: Zhu
authors.forename: Fanggang
authors.initials: F
authors.lastname: Bi
authors.forename: An
authors.initials: A
authors.lastname: Liu
authors.forename: Xiaozhou
authors.initials: X
authors.lastname: Ying
authors.forename: Haixiao
authors.initials: H
authors.lastname: Liu
authors.forename: Kehe
authors.initials: K
authors.lastname: Yu
authors.forename: Shigui
authors.initials: S
authors.lastname: Yan
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D006801:Humans; D008070:Lipopolysaccharides / Q000633:toxicity*; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000378:metabolism; D012645:Selenomethionine / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects* / Q000502:physiology; D020298:U937 Cells
chemical_list: D000893:Anti-Inflammatory Agents; D008070:Lipopolysaccharides; D016328:NF-kappa B; D012645:Selenomethionine