Fosinoprilat alleviates lipopolysaccharide (LPS)-induced inflammation by inhibiting TLR4/NF-κB signaling in monocytes
| Autor: | Weiyi Fang, Shuansuo Yang, Zengyong Qiao, Jiangwei Ma, Lei Tang, Xinkai Qu, Yue-Mei Hou, Guanghao Ge, Ruogu Li, Huajin Liu |
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| Rok vydání: | 2013 |
| Předmět: |
Lipopolysaccharide
Blotting Western Interleukin-1beta Immunology Angiotensin-Converting Enzyme Inhibitors Inflammation Biology Real-Time Polymerase Chain Reaction Monocytes Cell Line Flow cytometry chemistry.chemical_compound Fosinoprilat medicine Humans RNA Messenger medicine.diagnostic_test Interleukin-6 Tumor Necrosis Factor-alpha Monocyte NF-kappa B Interleukin Flow Cytometry Molecular biology Toll-Like Receptor 4 medicine.anatomical_structure chemistry TLR4 Fosinopril Tumor necrosis factor alpha medicine.symptom Signal Transduction |
| Zdroj: | Cellular Immunology. 284:182-186 |
| ISSN: | 0008-8749 |
| Popis: | Objective To evaluate the effect of the fosinoprilat on lipopolysacharides (LPS) induced inflammation in monocytes in vitro . Methods Human mononuclear THP1 cells were cultured in complete medium, treated with or without LPS and different concentrations (0, 0.25, 0.5, 1, 5, and 10 μmol/L) of fosinoprilat. Toll-like receptor (TLR4) mRNA expression was detected by real-time RT-PCR and TLR4 protein level on the surface of monocyte was determined by flow cytometry. Nuclear factor-kappa B (NF-κB) protein level was detected by Western blotting. Cultured supernatant of the THP1 cells in different groups were analyzed by ELISA to detect the levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF-α). Results Both the mRNA and surface protein level of the TLR4 in the THP1 cells were enhanced by the LPS treatment and down-regulated by pretreatment of the fosinoprilat. Accordingly, LPS-induced NF-κB protein was decreased by the fosinoprilat treatment. The increasing secretion of IL-1β, IL-6 and TNF-α induced by LPS could also be attenuated by the fosinoprilat treatment. Conclusion The inhibitory effect of the fosinoprilat on the TRL4/NF-κB signaling pathway reveals a potential anti-inflammatory and anti-atherosclerosis target. |
| Databáze: | OpenAIRE |
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